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Results : Mean age on onset for cases was Cases were, on average, less likely to smoke, and drink more coffee compared to controls. Cases and controls had similar body mass index distribution. Nine cases and five controls reported stimulant use. The OR for use of stimulants was 2.

Conclusions : While the association between stimulants and an increased risk of Parkinson's disease was similar to recent studies, we cannot rule out chance in this study. Background : RLS is a common disorder with prevalence rates between 5 to 30 percent. Methods : Number of people, above 15 years of age, living in Ankara was at the time of the study. We made contact with persons from randomly selected addresses from eight administrative districts of the city. Anyone who gave a positive response to any of the four questions were invited to hospital by telephone and evaluated by two neurologists based on the standard diagnostic criteria suggested by the International Restless Legs Syndrome Study Group IRLSSG.

Results : Among persons answered yes to any one of the screening questions, of them were unavailable to our telephone calls, and among persons who could be reached by telephone, 39 were diagnosed to have RLS 32 females, 7 males. So the prevalence of RLS was 5. This rate is quite similar to other studies from Turkey 3. The prevalence rate is somewhere between western and eastern world as is the geographical location of Turkey. Objective : To evaluate the association of farming and the incidence of Parkinson's disease PD in Austria. Background : Rural living has long been debated as a risk factor for PD.

A few epidemiological studies have implicated the use of pesticides in farming with the incidence of idiopathic PD, however these data are considered incomplete and are therefore regarded controversially. These figures were correlated with the agricultural index in each district, which expresses the share of agricultural employment. Results : For the investigated year , we identified This yielded a hospitalized patients prevalence of per We found a highly significant positive correlation between these parameters, i.

Conclusions : The significant association between the prevalence of PD and the agricultural employment in Austria supports the view that agricultural toxins or other factors associated with an agricultural lifestyle might be involved in the pathogenesis of this disease. Objective : To determine whether there are cognitive deficits in early Parkinson's disease PD patients and whether there are deficits other that executive dysfunction. Background : Executive dysfunction has been shown to be associated with PD later in the disease process. However, few studies have looked at other cognitive deficits in PD patients, such as parietal and temporal lobe dysfunction.

Further few studies have analyzed cognitive deficits early in the disease process. Methods : Neuropsychological evaluations were retrospectively analyzed for genetic and idiopathic PD patients. Results : Integrated Visual and Auditory Continuous Performance tests of Auditory Stamina, and Auditory Vigilance and Controlled oral Word Association tests showed a trend for a significant difference between the groups [table 1].

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Wechsler Memory Scale Logical Memory Percent Retention was the only score that showed a significant difference between groups [table 1]. Consistency, Vigilance, Focus, and speed were also below average. Physicians should consider running more extensive cognitive testing batteries on PD patients earlier in the disease process. Objective : Aim of this study was to evaluate the impact of sleep disturbances on decision making in non demented Parkinson's disease PD patients compared with Sleep Apnea Syndrome patients OSAS , by using a virtual immersion in a supermarket.

Also patients with OSAS may often complain attention and memory deficit, clinically correlated with diurnal sleepiness. The MET is an assessment of executive functions in daily life and consists to perform tasks according predefined rules, so that there are items to be bought and informations to be obtained.

By comparing with controls, while OSAS patients showed no significant differences, PD patients showed significant lower performances in the virtual strategies. Muchmore, the defective strategy in a virtual supermarket was significantly correlated with polysonnographyc abnormalities. Objective : To evaluate the effects of concomitant cognitive tasks of increasing difficulty on speed of cycling in people with Parkinson's disease PD. Background : Studies have demonstrated that compared to healthy older adults, people with PD show greater declines in motor performance gait, balance when simultaneously performing a second task, regardless of the domain of the second task motor, cognitive, language.

Cycling reduces fall risk and thus may better assess true dual task interactions. We predicted that there would be a direct and graded effect of cognitive task difficulty on cycling performance. Cycling speed RPMs was recorded with no cognitive task baseline and during each cognitive task. Cognitive tasks were chosen from 5 domains of increasing difficulty: processing speed, controlled processing, memory, executive function, and language. Results : Unexpectedly, in nearly all tasks, cycling performance RPMs improved in the dual task. Dual task benefits during controlled processing tasks were also significant, but those for memory and the most difficult executive and language tasks were not.

Conclusions : We posit two interacting processes. Kinesia paradoxa is a phenomenon in which motor performance in PD is facilitated by external stimuli a line on the floor, a metronome. This may be the first report of kinesia paradoxa resulting from cognitive, rather than sensory, stimuli. The second process was a typical dual task effect but from the improved dual task level rather than baseline , that showed a graded increase in dual task costs on motor performance as cognitive task difficulty increased across a broad range of cognitive domains.

Background : Cognitive impairment is an important issue in PD. A brief screening instrument for global cognitive function is needed to aid comprehensive management of patients. In the PD group the mean age SD was The mean age of controls was Objective : To find an association between gait pattern and specific cognitive profiles in patients affected by Parkinson's disease PD. Background : Although recently the relationship between cognition and gait in PD has received increasing attention, the specific connections between gait pattern and cognitive features are not fully understood 1.

Methods : Using a gait analysis system, we studied 43 PD patients during normal gait at on state. In order to reduce the larger number of gait variables to a smaller number of factors, a factor analysis was performed. Furthermore, we assessed all patients with an extensive neuropsychological battery and correlated the composite scores of three main cognitive domains, namely episodic memory, executive and visuospatial domains with the gait factors scores.

Conclusions : Visuospatial impairment was strongly associated with the development of instability and more generally with the progression of PD. The role of executive function and attention in gait. These examinations were conducted preoperatively and 1 year postoperatively. Moreover, lowering of the word fluency test score was detected, similar to previous reports.

Objective : We assessed whether there is a negative effect on cognition of clinical autonomic dysfunction in PD patients. Background : Parkinson's disease PD is a chronic progressive neurodegenerative disorder characterized by tremor, rigidity, bradykinesia, and postural instability. PD also involves nonmotor manifestations such as autonomic failure, cognitive disorders, and sleep disorders.

These clinical characteristics are not identical in severity, frequency, and onset time in all PD patients. Methods : This prospective study includes 37 PD patients with autonomic failure. Conclusions : According to our results, clinical autonomic dysfunction did not seem to have an effect on cognition. In addition, severity of cognitive dysfunction showed a strong negative correlation with the stage of disease.

The question why patients develop CI or D, and the longitudinal course and trajectories are poorly understood. Thus, the DEMPARK study is to determine incidence and prevalence of cognitive impairment, dementia and their risk factors in a large cohort of PD patients and to examine their developmental pathways and trajectories. Mean age of the participants Disease duration at enrolment was 7.

At baseline, Conclusions : Preliminary DEMPARK baseline findings indicate that the study program is feasible and should allow to identify putative trajectories of cognitive decline over the total observation period of 24 months. Methods : Parkinson's disease PD subjects were recruited from those scheduled for neuropsychological testing at two specialty PD centers. All subjects were categorized as having PDD or no PDD based on routine neuropsychological test results and clinical judgment of the neuropsychologist.

Results : We tested 91 PD subjects, with mean age These 6 cases had more significantly more education Conclusions : MDS Level II criteria diagnoses PDD more frequently compared to routine neuropsychological testing and may be more sensitive to impairment in cases with higher education levels and where the cognitive function is not as severely impaired. Objective : The aim of this study was to compare the effectiveness of gait training associated with executive function EF tasks versus gait training alone, for improving gait, motor learning and transfer in PD patients. The PD patients have both gait and cognitive disorders, so the development of a gait training which involving these domains should be interesting in attenuate these deficiencies, and enhance performance in this group of patients.

Methods : A blinded, randomized, controlled, longitudinal clinical trial was conducted. Both types of training session were preceded by 30 minutes of general mobility exercises. In the GT, gait was trained in the same manner and for the same period but with no associated tasks. Patients from both groups were instructed to walk as quickly as possible. The sessions 1, 5 and 10 were included for statistical analysis. Additionally, PD patients were able to transfer the improvements in performance in only some tasks, for some cognitive and motor tests.

This appears to be associated with deficiency in EF, such as divided attention, working memory and decision making. Objective : To identify specific cognitive deficit profiles in an incident cohort of PD patients. We compared the groups in terms of age, education, gender, disease duration and motor characteristics e.

Results : Within the whole PD cohort [age: Conclusions : Our results suggest that specific cognitive profiles canbe identified in PD and they may help predicting the emergence of cognitive changes. Objective : To examine the role of dopamine among patients with Parkinson's disease PD in their ability to judge harmful intent actions as morally inappropriate. Background : Judging an action as morally right or wrong demands that we infer the feelings, beliefs, and intentions of the actor. Each vignette introduced an actor executing an action with either neutral intent e. Sally added sugar to Kelly's coffee or harmful intent e.

Sally added poison to Kelly's coffee and either a neutral outcome e. Kelly was fine or a negative outcome e. Kelly died. For each vignette, participants were asked to determine 1 how morally appropriate or inappropriate the actor's action was; and 2 how severely the actor deserved to be punished. Vignettes were presented in counterbalanced order. Levodopa test to ensure that results were independent of the dopaminergic agonist administered.

We then analyze the way in which responses to moral vignettes were modulated by the action of dopamine in an OFF vs. ON analysis. We especially focus in the way PD patients' ability to detect harmful intent actions as morally wrong changes during the ON phase relative to the OFF phase. Conclusions : Decreased dopamine levels in PD appear to be associated with a diminished ability to infer other people's beliefs and intentions.

This, in turn, influences the way in which PD patients judge immoral actions as inappropriate. The present study highlights not only the potential role of dopamine in higher cognitive functions, but also the wide array of social cognitive functions that may be disrupted in patients with PD. These differences may have important consequences on motor performance and motor control. For instance, PIGD patients are characterized by propensity for falls, and patients seem to react impulsively to their environment.

In the current investigation, we tested the hypothesis that PIGD patients show reduced cognitive control over motor impulses compared to TD patients. All patients performed the Simon task, which requires speeded manual reactions to stimuli presented on a computer screen. Patients were considered to have mild to early moderate symptom profiles. Both groups showed similar mean reaction times, but compared to TD patients, PIGD patients made significantly more impulsive motor errors.

Notably, when the initial impulsive response was avoided, PIGD and TD groups were similar in their ability to suppress the incorrect motor impulse from interfering with the selection of a correct action. This finding may have direct implications for fall risk and point to dissociable neurocognitive phenotypes in TD and PIGD subtypes. Clinically, the use of specific cognitive instruments to assess the expression and inhibition of motor impulses may help identify PD patients at a high risk of falling. Background : One of the major issues for the diagnosis of dementia in PD is to establish that the cognitive impairment caused significant disability, because it can be difficult to distinguish between the functional restriction due to motor signs and the disabilities due to cognitive impairment.

The PFAQ is an instrument used to grade functional loss in patients with dementia. Methods : It has been examined 58 of patients with PD consecutively seen at a movement disorders outpatient clinic, as they were followed by a close caregiver which could inform accurately about the cognitive abilities of the patients.

Conclusions : Defining disability due to cognitive impairment is a difficult assignment in PD patients, however, the PFAQ seems to be a good tool for such task. Objective : To determine whether elevated plasma homocysteine Hcy levels impact upon cognition in early Parkinson's disease PD. Background : Elevated plasma Hcy is a risk factor for cognitive dysfunction and dementia in the general population.

Elevated homocysteine levels have been associated with motor and cognitive decline in established PD and predict a poorer response to rivastigmine in those with PD dementia. Plasma levels of Hcy, vitamin B12 and folate were analysed. Linear regression was used to examine the relationship between Hcy and cognition with age, education, folate and vitamin B12 as covariates.

Results : Hcy was significantly higher in PD The results are shown in table 1. Conclusions : Our findings indicate that homocysteine is elevated even in the earliest stages of PD and predicts worse cognitive function. This cohort will be followed up over the next 3 years to determine the significance of Hcy in predicting cognitive decline. Further work is needed to establish whether Hcy is a potentially modifiable risk factor for PDD. Objective : 1 To highlight psychomotor slowing in Parkinson's disease PD patients, 2 to determine the underlying mechanisms and 3 to determine whether levodopa medication influences reaction time.

Background : Although psychomotor slowing is well documented in Parkinson's disease, few studies have focused on its pathophysiological mechanisms. Determine its mechanisms is now possible with a validated and reliable battery assessing the speed of the four components of reaction time perceptual, motor, decision and attention processes. Methods : We recruited 20 patients with PD and 20 controls matched for education and age.

First of all, we examined the performance of both groups on psychomotor speed with simple reaction time SRT simple and dual task , digital tapping, choice reaction time CRT and visual inspection time VIT tasks. Results : PD patients were not different from controls. No significant improvement in reaction time performance was seen after administration of dopaminergic medication. Conclusions : Psychomotor slowing of PD is due to slower motor and decision processes. This psychomotor slowing profile could constitute a diagnostic marker in PD.

However the cognitive profile is less well characterized. A comprehensive neuropsychological battery of neuropsychological test was administered for assessing general cognition, attention, executive function, memory, language, visuoperceptive and visuospatial skills, and emotion recognition. Results : There was not any significant difference in demographic variables and education level in the two groups.

Neuropsychological assessment included general cognition evaluation, attention, working memory and executive function, memory, visuospatial function, and emotion recognition. We didn't found any significant difference in neuropsychiatric scales between groups. Longitudinal data are needed to confirm these results and to unravel their meaning.

Objective : To evaluate the effect of reward and punishment on probability learning in patients with Parkinson's disease as compared to healthy controls. Background : Impairment in implicit learning has been demonstrated in patients with Parkinson's disease. Yet it remains unclear, if this impairment is due to a disability in acquisition of content or a difficulty in processing of feedback. If processing of feedback is impaired it remains to be elucidated, whether positive as well as negative feedback is affected. Results : Parkinson's patients with dopaminergic medication were not impaired as compared to healthy controls in learning from negative feedback.

However in trials with positive feedback patients showed a significant impairment in learning. Conclusions : Our data show an impairment of reward learning in patients with Parkinson's disease even when dopamine is substituted orally. However, this does not seem to reflect a general impairment of content acquisition or processing of feedback in general, but rather seems to be specific for learning from positive feedback.

Objective : To study the progression of cognitive deficits in PD patients with MCI and with normal cognition and to identify risk factors for cognitive decline. Background : Dementia is frequent in Parkinson's disease PD. Mild cognitive impairment MCI is a risk factor for dementia but little is known about the progression of cognitive deficits in this population of PD patients. Patients were older than 60 years and the disease duration was of at least 10 years. An extensive neuropsychological evaluation was undertaken.

Univariate analysis was done to study the evolution of cognitive test scores and cognitive domains. Afterwards a logistic regression matched by age, sex and educational level, was applied to determine associated risk factors for progression of cognitive deficits. A trend towards significance was also observed for low scores in the copy of intersecting pentagons. Conclusions : After 2. Postural instability and poor attention and visuospatial function seem to be risk factor for the progression of cognitive decline. Objective : In this study, we report how pharmacological treatment in Parkinson's disease PD affects neural circuitry involved in spatial working memory processing and how it affects spatial working memory performance.

Background : An important feature of PD is the emergence of cognitive deficits. However, findings of previous cognitive studies have not been consistent and the specific effects of levodopa on cognition remain unclear. Methods : We combined two studies. Levodopa had a differential effect on task performance in that it was dependent on working memory performance in the untreated state. Those patients with low working memory performance when off improved after levodopa, and those with high working memory performance when off deteriorated after levodopa.

Levodopa may, therefore, enhance spatial working memory in some and impair it in other patients. Background : Sleep disturbances are common in PD and contribute to worse cognitive performance. While many studies focus on global PSQI scores, evaluation of sleep quality components may elucidate contributors to poor sleep quality in PD and their relationship to cognition.

Relationships between sleep and cognitive measures were examined with Spearman correlations. Global PSQI scores did not differ significantly among cognitive groups. Conclusions : PD subjects with greater cognitive impairment exhibit a profile of longer sleep duration and possible greater daytime dysfunction.

Global sleep quality, however, is impaired in most PD subjects, regardless of cognitive status. Background : Individuals often must coordinate with others when making decisions. Coordination is supported by executive and theory of mind resources mediated by prefrontal cortex PFC; McMillan et al.

In the Survey condition, participants could provide any response. In the Coordination condition, participants were asked to respond with the same answer they think an anonymous partner would give. Responses were quantified using a measure of semantic representativeness, the focal index FI; e. Cognitive testing and volumetric MRI analysis were related to coordination performance. Regression analysis related coordination deficits to atrophy in left rostral PFC BA 10 , as well as the right insula and right occipital lobe.

Mehta et al. Focal points in pure coordination games: An experimental investigation. McMillan et al. The neural basis of establishing a focal point in pure coordination games. Soc Cogn Affect Neurosci , in press. Background : A wide range of cognitive functions seem to remain stable after DBS in the STN, however performance in verbal fluency tasks have been shown to decrease 6 to 36 months after surgery Witt et al. Conclusions : No clinically significant worsening could be observed in both fluency tasks.

These preliminary results suggest DBS to be relatively safe regarding dysfunctions in vulnerable executive functions. Objective : To look at the common practice in Movement Disorders clinics across the country regarding cognitive screening and tools used in patients with Parkinson's disease. Patients with PD for greater than one year, attending the Movement Disorders clinic was included. Their medical records were surveyed for cognitive screening and the tool used. Results : of patients Conclusions : Cognitive screening was done only in Evolution of cognitive dysfunction in an incident Parkinson's disease cohort.

Epub May J Am Geriatr Soc. We have a chance to investigate psychiatric symptoms in PD. Our aim of this study is to develop strategy for making an improvement or for maintaining the psychiatric conditions in PD. Methods : Our survey was carried out after our Hospital Ethics Committee approved our clinical research program.

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We used the methods of questionnaire and interview technique for psychological examination by skillful clinical psychotherapists. These data were analyzed by adequate statistical methods. Results : 1. From the results of RBMT, verbal memory is well preserved compared with spatial and prospective memory. Conclusions : In this investigation, characteristics of psychiatric symptoms in PD become identified.

Objective : To examine the effects of performing simultaneous cognitive and motor tasks on cognitive performance executive function, processing speed, and working memory WM in Parkinson's disease PD. Background : While the effects of cognitive tasks on motor performance have been explored, the effects of concurrent motor tasks on cognitive performance in PD are not fully understood.

Response times on the Digit Symbol Substitution task exhibited a reverse dual task effect: faster response times during the dual task. Accuracy on the Operation Span also showed a reverse dual task effect, with better recall during the dual task. However, the visual WM task showed no dual task effects. Indeed, in both the single and dual tasks, participants performed at chance for the most difficult level of the visual WM task.

There was no evidence that cognitive tasks were prioritized over cycling. Conclusions : In contrast to a robust literature on healthy older adults that largely documents declines in cognitive performance during a simultaneous motor task, our findings in PD demonstrate that some motor dual tasks may differentially improve some but not all aspects of cognitive performance. We compared gait measures of PIGD vs.

Cognitive Cog function was evaluated using a computerized neuropsychological battery that generated indices for several Cog domains. PIGD had higher strcv 0. Moreover, these results demonstrate for the first time that PIGD apparently have less coping abilities during challenging walking conditions. Objective : The aim of this study was to test the performance of PD patients in naming static versus dynamic actions compared to controls. Recent findings have demonstrated a specific impairment in the processing of verbs in PD patients assessed by naming actions from pictures.

This effect could be explained according to the notion that the same prefrontal areas related to planning and execution of movements are involved in verb processing. Several studies have been conducted with static action pictures, but only a few comparing both static and dynamic actions; better naming performance has been found for static than dynamic actions in brain damaged people.

A set of 48 videoclips 4s duration and 48 real static photographs were selected.


The psycholinguistic variables of the verbs associated with the presented actions were matched. Results : We found that naming times tended to be slower for PD patients than controls for both, dynamic and static actions. However, these differences were significant only for naming dynamic actions. Conclusions : Our PD patients were significantly poorer at naming dynamic actions compared to healthy controls. This result suggests that PD patients may need more time to understand dynamic actions, which probably require extensive cognitive and premotor mechanisms. Background : White matter hyperintensities WMH in the cholinergic pathways show a stronger correlation with cognitive performance than general WMH in Alzheimer's disease.

However, the role of WMH within the cholinergic pathways in cognitive dysfunction has not been investigated in Parkinson's disease PD. Conclusions : This study demonstrated that the burden of WMH within cholinergic pathways was significantly higher in patients with PDD relative to other groups and that cholinergic WMH was significantly correlated with a decline in frontal executive function and attention.

Background : Ample evidence has suggested that individuals with subjective memory complaints are at a higher risk for cognitive decline. Nevertheless, the significance of subjective memory complaints in Parkinson's disease has not been studied until now. Methods : We investigated whether the patterns of cognitive profiles and gray matter density differed in cognitively normal patients with Parkinson's disease based on the presence of subjective memory complaints.

Results : No significant differences in demographic characteristics were observed between groups. MoCA may be more sensitive than MMSE, but its positive predictive value relatively low in populations of low edication. Quantitative assessment of it by command and by copy condition is reported to be sensitive for temporal and frontal, and parietal dysfunction, respectively. CDT was quantitatively assessed by both command and copy conditions according to the methods of Rouleau The cognitive impairment was defined by diagnostic criteria of dementia in PD blinded to the results of the 3 screening tools.

Results : The mean age and the duration of PD was 69 and 4. The mean educational year was 7. Objective : To study the clinical and neuropsycological profile in Parkinson's disease patients at a tertiary care referral centre. Methods : Forty one patients with a clinical diagnosis of PD who were of 20 years of age and above, had completed their primary education, were enrolled. Results : Out of a total of 41 patients included in our study 30 were male it included 11 females. Majority of the patients 20 Neuropsychological testing revealed that the mean T scores of the lobar scales both right and left hemispheres in patient group LF — Conclusions : Thus our study revealed significant impairment of lobar functions in patients with PD with predominantly right hemispheric dysfunction in patient's stage 2 and above.

Objective : To assess the longitudinal course of cognition in elderly women diagnosed with Parkinson's disease PD. However, few studies have investigated the longitudinal course of cognition in PD, especially among older women. Methods : We studied older women mean age 71 years at baseline who were followed for up to 18 years as part of the ongoing study.

In addition, participants completed an expanded cognitive battery at a final visit 18 years after baseline. Cognitive trajectory slopes were modeled with an inflection for report of PD if made after baseline. Repeated measures regression analyses were used to calculate cognitive trajectory slope on Trails B or MMSE over 18 years; models were adjusted for age, education, and depression.

Results : Of the women, 3. These results may have implications for the underlying longitudinal neuropathological characteristics in this population. There were 78 men and 46 women with a mean age of Performance in the DRS test was equal in both groups Conclusions : Our results do not support the hypothesis that Brain Derived Neurotrophic Factor ValMet polymorphism plays a major role in cognitive function in PD patients. Objective : To investigate the correlation of pill questionnaire on cognitive function and activities of daily living ADL in patients with Parkinson's disease PD.

Background : Pill questionnaire has been proposed as a simple questionnaire for assessing decline in cognitive function and its impact on daily live in PD. This is very easy to administer, however there is little evidence on the correlation of other screening instruments. In this paper, we evaluated the correlation between the pill questionnaire score and cognitive deficit and impaired ADL. The statistical analysis was performed for comparison of the variables' mean between them.

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Correlations of pill questionnaire scores, cognitive impairment variables, ADL, and PD severities were determined using logistic regression models. Results : A total participants 93 men were included. The average score of the MoCA was The groups differed significantly for all cognitive measures and motor severities. Correlation analysis showed that pill questionnaire appeared to represent ADL. Conclusions : Pill questionnaire is a sensitive and useful test for detecting cognitive impairment and its impact on daily living in PD.

Objective : To investigate 1 the clinical factors affecting dysphagia and 2 the relationship between cognitive impairment including dysexecutive function and dysphagia in Parkinson's disease PD. Background : Swallowing difficulty is frequently observed in PD patients and the risk of aspiration pneumonia in patients affects the quality of life. Multiple clinical factors associated with PD including cognitive function are supposed to influence dyphagia.

More pronounced frontal dysexecutive function in PD may play a significant role in swallowing function. Motor series programming and prehension behavior environmental autonomy subscores of FAB are correlated with the severity of dysphagia. Conclusions : Swallowing difficulty occurs more frequently in the patients with severe motor symptom and cognitive impairment.

Frontal dysexecutive symptom is shown to disturb the proper eating process from oral to pharyngeal stage. Early detection of dysphagia in patients with silent aspiration seems to be necessary and the rehabilitating therapeutic strategy enhancing motor and cognitive function together may help the swallowing ability in PD. Objective : To evaluate the presence of cognitive impairment in Parkinson's disease PD using the minimental Parkinson's scale, the clock drawing test and the generation of words by category and code. The patients were dated early in the morning and at the same time they took their medication.

After 30 minutes of the intake of treatment it was performed the minimental Parkinson's scale, The clock drawing test CDT by copy and order, and finally the generation of words in 1 minute by category semantic and by code phonologic. We performed univariate and bivariate statistical analysis data in SPSS Conclusions : Patients with PD do have cognitive impairment as we found in this pilot study, having a relationship with age and schooling years, as we saw specially when performing the generation of words by code in 1 minute, which talks about frontosubcortical impairment, as seen in PD. Objective : The purpose of this study was to address the question whether COMTvalMet genotype would be associated with performance in Executive function tests in Parkinson's disease PD.

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This polymorphism has been associated with frontal lobe function in normal subjects and in a variety of disorders including PD, but the literature data on this relationship are contradictory and inconsistent. Methods : The study population consisted of PD patients 77 men and 53 women with a mean age of There was no difference in WCST pertinent outcome measures between the three groups.

However this subtle difference did not affect the whole WCST performance. There was also no difference in the performance on the WF task or the Trail Making test. Results : The morphometric analysis showed that patients with earlier cognitive decline demonstrated greater cortical atrophy in the inferior parietal and orbitofrontal areas than did those with later cognitive decline. Additionally, the anatomical bases of the timing of their cognitive declines differed in terms of correlation patterns.

Conclusions : These data suggest that the pathological burden in Parkinson's disease with mild cognitive impairment may be more severe in patients with earlier cognitive decline than in those with later cognitive decline and that the neural basis corresponding to the timing of cognitive decline may differ in these patients. Results : The MoCA was more sensitive in identifying cognitive deficit, specifically in the domains of visuospatial abilities, language, and memory. The MoCA, however, did not change significantly, regardless of disease duration, even when subjects were stratified by age, MMSE score, and time in the study.

Conclusions : This suggests the MoCA warrants further study in assessing its value for longitudinal study, such as for use in clinical trials. A subset of patients underwent a review of the above tests and assessment of level of functional impairment from cognitive dysfunction, by a consensus panel of at least two neurologists and a neuropsychologist, and received a diagnosis of no cognitive impairment, dementia, or cognitive impairment with no dementia. The greatest impairments were found on Trails B and Digit Symbol.

Objective : To develop a neuropsychological test battery that promotes and assists in collaborative studies of cognition in Parkinson's disease PD. Background : Cognitive impairment and behavioral disturbances can be the earliest symptoms of PD and afflict the vast majority of patients as disease progresses. Together, cognitive impairment and behavioral disturbances account for increased disability for patients and greater burden for caregivers. Despite their prevalence and significance in PD, cognitive impairment and behavioral disturbances are only recently a focus of investigators.

Methods : Two Morris K. Udall Centers of Excellence for Parkinson's Disease Research, with a focus on these common and devastating features of PD, were supported by the National Institute of Neurological Disorders and Stroke NINDS in an effort to devise a comprehensive yet readily usable cognitive and behavioral assessment battery to fuel collaborative research.

Results : We devised a tiered approach of four levels of evaluation that is based on the most recent scholarship and that is suitable for studies with varying emphasis on cognition and behavior. Our approach is intended to be flexible and not place undue burden on participants or research resources. We sought a high degree of compatibility with existing test batteries to promote collaboration not only across our Udall Centers but also other national research programs focused on PD as well as other neurodegenerative diseases.

Conclusions : We hope this approach will promote collaborative research across multiple institutions and centers, and thereby accelerate research progress into cognitive and behavior changes in PD and related disorders. Impact on ADL function is often judged by caregivers. Besides cognitive impairment, motor worsening might influence patients ADL ability.

Results : Thirty patients Nearly all patients It can accompany the progression of motor disability and titration of dopaminergic therapy. Psychosis can be distressing to both patient and carer, whilst increasing the need for placement in nursing care. Limited evidence is available to guide management of psychosis in PD. Scottish Intercollegiate Guidelines Network SIGN recommends initially identifying and modifying any contributing factors, followed by reduction in dopaminergic therapy. If antipsychotic therapy is required, low dose clozapine with monitoring of white cell count is recommended as the first line.

If blood monitoring is not possible, low dose quetiapine is recommended. There were 47 responses 19 consultants, 14 PDNS, 15 trainees. Conversely Respondents reported clozapine is not used routinely due to concerns about the side effect profile, intensive monitoring and lack of drug familiarity. This is due to service and clinical issues. Closer collaboration with old age psychiatry may improve the service for people with PD and their carers. In particular, olfactory dysfunction appears to be one of the earliest signs of several neurodegenerative disorders such as Alzheimer's disease and PD.

Olfactory dysfunction is present in the majority of PD patients and often precedes the onset of motor manifestations. Methods : patients were evaluated at the Parkinson's Disease Clinic at the National Institutes of Health, National Institute of Neurological Disorders and Stroke with a detailed neurological evaluation. Men had worse olfactory function than women. Conclusions : Olfactory function is correlated with fatigue and cognitive function as well as age and motor function. Objective : To examine 1 visual sampling during walking in PD under different levels of environmental complexity and 2 associations between saccadic outcomes and clinical measures.

Background : Gait disturbance is intrinsic to advanced Parkinson's disease PD , but its aetiological basis is incompletely understood. Visuospatial dysfunction may play a crucial role, in particular how visual exploration of the environment is integrated into gait control. Participants walked under four environmental conditions during single and dual task. Saccade frequency and timing, and task duration were measured. Conclusions : People with PD explore their environment less frequently than controls and are unable to alter the timing of saccades in response to environmental features.

Lack of visual adaptation may contribute to the gait disorder of PD. Background : Although being an effective treatment option for advanced Parkinson's disease PD , deep brain stimulation DBS of the subthalamic nucleus STN can alter cognitive and affective functions. Results : Preliminary data from an ongoing trial are reported. Patients exhibited slower reaction times in the ST compared to controls.

DBS appears to shift the balance between cognitive flexibility and stability in the direction of enhanced stability. Findings could be interpreted within the functional profile of the STN for phasic behavioural inhibition. Objective : To estimate the prevalence of olfactory dysfunction OD in patients with Parkinson's disease PD attending a specialist clinic and to assess its relationship with motor, autonomic, and cognitive dysfunction. Background : PD patients can exhibit OD in several modalities, especially in odor identification tests.

Failure in any of four items banana, gasoline, cinnamon, chocolate perfectly discriminated the two groups. The presence of subjective complaints had a high positive predictive value 0. The presence of OD was associated with a worse performance in motor and cognitive tests but not in autonomic tests. Hence, there is a need for screening tests in this setting. Multivariate logistic regression analysis was used to define predictive models for the presence of CI or DEM. The multivariate predictive model for DEM included the HY stage and the presence of complaints; the model for CI also included the educational level.

Objective : The aim of our study is to identify presenting symptoms in patients with Parkinson's disease and frequency of memory impairment among these patients. Background : Dementia was the term first introduce over years ago. The diagnosis of dementia requires the development of multiple cognitive deficits that are sufficiently severe to cause impairment in occupational or social functional. Dementia is increasingly recognized as an important feature of PD in the elderly. The demographic characteristic and clinical presentation of the disease pattern were recorded.

The data collected was analyzed on SPSS version Out of 35 cases six We divided the sample into two groups on the basis of presence and absence of dementia features among the patients. Most having PDD started their Parkinson's symptoms of dementia after the 6 the decade. Conclusions : Dementia in Parkinson's disease was at the Department of Neurology Jinnah Postgraduate Medical Center Karachi not quite high in our study as compared to the western studies but having a significant percentage with the male predominance. Objective : To evaluate the correlation of kinematic parameters of upper limb motor performance with brain dopaminergic function in Parkinson's disease PD.

When compared to normal controls, PD patients present a reduced flexibility in selecting the time required to perform movements to predictable versus unpredictable targets. This has been related to a reduced kinematic flexibility and involvement of the direct pathway Moisello C et al. Parkinsonism Relat Disord. Results : Indexes of motor performance such as reaction time, movement time, spatial accuracy in reaching the target were computed. No significant correlation was found between FluoroDOPA uptake and reaction time, movement time and spatial accuracy.

Conclusions : Our data try to contribute in understanding the novel concept of kinematic flexibility in PD and point to the involvement of lateral temporal cortex in this peculiar function in early PD. PD patients performed the protocol after 12 to 18 hours of parkinsonian medication withdrawal on two occasions, before and after levodopa administration.

Results : Significant increases in activity in the cerebellum were observed for SI compared to ET movements for all groups of participants. Compared with healthy volunteers, PD patients off medication revealed decreased activity in the premotor cortex, the striatum and the cerebellum for SI and ET movements.

PD patients' activity in the striatum and the cerebellum was significantly increased after levodopa administration. Levodopa has a strong effect not only on the basal ganglia, as expected, but also on the cerebellum. Methods : Nine hundred ninety two patients with PD from six sites in the U. The entire GBA coding region was screened for mutations in all patients.

Linear regression was used to test for association between mutation status and raw scores on all tests adjusting for sex, years of education, and disease duration. Results : Pathogenic GBA mutations were identified in 42 of 4. Conclusions : In contrast to previous reports using limited cognitive data, our findings based on detailed psychometric testing suggest that in PD patients GBA mutation status does not influence cognitive performance or risk for CI. Methods : We recruited PD patients from six academic centers in the U. Linear regression was used to test for association between genotype and cognitive performance at baseline adjusting for sex, years of education, disease duration, and age at testing.

The latter observation suggests that SNCA is both a susceptibility gene for PD and modifier of cognitive function in patients with an established diagnosis of PD. Objective : To indicate the possible association between Parkinson's disease PD and Capgras syndrome which could be a rare psychiatric manifestation of PD. Background : Capgras syndrome is a delusional phenomenon in which the patient believes that a closely related person has been replaced by one or more impostors.

This rare syndrome has initially been observed in psychiatric disorders and more recently has also been described in some neurological conditions especially in head trauma and neurodegenerative diseases such as Lewy body dementia. Initially he exhibited unilateral rest tremor, bradykinesia and rigidity and had a good response to dopaminergic therapy. After two years he developed visual hallucinations seeing little children , which responded to discontinuation of dopa agonist and its replacement with levodopa. One year ago the patient visited his son in USA and there he became confused believing that his family was replaced by impostors.

The patient had a mild dementia. Neuropsychological testing demonstrated impaired visuospatial and visuomotor abilities, dysexecutive syndrome, attention and concentration difficulties and mild memory impairment. Brain MRI , revealed mild brain atrophy and leukoencephalopathy of unclear origin comprehensive clinical and laboratory investigations had been performed. Treatment with rivastigmine and quetiapine slightly improved his Capgras syndrome. Conclusions : It is well known that patients with PD have a high incidence of psychiatric symptoms like hallucinations, depression, anxiety, sleep disturbances and repetitive behavior.

To our knowledge, Capgras syndrome has been rarely reported in PD. Every patient with PD and Capgras syndrome should be thoroughly examined to rule out any other possible cause of this delusion. Objective : To predict Parkinson's disease PD patients at high and low risk of severe cognitive decline using serial MRI scanning across two years. Background : We need to identify patients with PD at imminent risk of dementia so they can be appropriately targeted in forthcoming therapeutic trials.

Recent developments in other disorders suggest that serial MRI may provide effective prediction of cognitive decline. Participants also completed neuropsychological and motor assessment at both timepoints. Perfusion values were extracted from occipital and posterior parietal cortex. We hypothesized that, according to the motor and cognitive demands of the games selected, patients with PD, after extensive training, would be able to learn, retain and transfer to a similar motor task, with or without impairments, compared to healthy elderly.

The training was split into 14 sessions with two sessions given per week. Results : Patients with PD showed no deficit in learning or retention on 7 of the 10 games, despite showing poorer performance on 5 games in comparison to healthy elderly. Patients showed marked learning deficits on 3 other games, independently of poorer initial performance. This deficit appears to be associated to cognitive demands of the games which require decision making, response inhibition, divided attention and working memory.

Finally, PD patients were able to transfer performance improvements on games to the functional reach test. Conclusions : The ability of PD patients to learn, retain and transfer performance improvements after training on the NWF depends largely on the demands, particularly cognitive, of the games involved, reiterating the importance of selecting games for rehabilitation purposes.

No objective biomarker reflects disease progression. All subjects underwent neuropsychological testing, collection of biological fluids blood, cerebrospinal fluid, urine, etc. The cohort will be followed for several years with investigations every two years. Results : We will report the entire baseline data. Hoehn and Yahr stage in PD subjects ranged between 1 and 3 mean: 1. Neuropsychological testing, smell testing, midbrain ultrasound and polysomnography revealed significant differences between PD and HC subjects.

Conclusions : The imaging and behavioural data indicate that the effect of the COMT polymorphism may be dependent on specific components of cognition, while the DAT1 one may reflect a more global cognitive profile in PD. However, no study to date has explored whether these attentional deficits are directly related to the severity of actual FOG episodes. Percent time frozen, previously demonstrated as a more robust FOG metric than number of events [Shine et al.

Results : Poorer performance on the trail making test was significantly correlated with increased severity of freezing of gait during the locomotion task. TOL task of planning is associated with activation of including bilateral frontopolar, dosolateral prefrontal DLPFC and posterior parietal cortex. Preprocessing and imaging analysis used Statistical Parametric Mapping 8. There were no significant differences between PD patients and controls in the activations associated with Planning vs Count trials.

Conclusions : PD patients in the earliest stages show normal activation of a frontoparietal network during planning on the TOL task. Behavioural and fMRI results were reproduced at two sites, with no significant differences. These results represent an important baseline from which to assess the development of cognitive decline and dementia in PD.

The neurocognitive profile and LID vary widely in type and severity. We sought to determine whether LID correlate with neurocognitive function.

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Phenomenology predominantly chorea vs. Results : patients were evaluated 77 M, 42 F; mean age, They were predominantly axial in 72 patients; exclusively appendicular in There were no differences in age, disease duration, LED and neurocognitive profile between those with and without LID. Conclusions : Correlation between distribution of LID and neurocognitive function is poor.

Objective : This study aimed to demonstrate anatomical and quantitative cerebral functional map in patients with Parkinson's disease PD , and to reveal its correlation with their cognitive impairment evaluated by Montreal Cognitive Assessment MoCA. Conclusions : The profile of cognitive impairment in PD evaluated by MoCA is correlated with hypofunction of particular cortical segments, providing physiological basis of MoCA in terms of cerebral cortical topography.

Background : Hyperhomocysteinemia HHcy associated with levodopa utilization may cause cognitive decline and thus complicate the clinical course of PD.

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  7. Fasting total plasma homocysteine Hcy levels were determined in all subjects. HHcy was defined as any level above the 90th percentile of Hcy values in controls. Cognitive impairment was defined as any score below 2 standard deviations of the mean composite score of MMSE and category fluency of controls i. Results : PD cases and controls were matched for age, gender and level of education. The PD cases had a mean age at onset of HHcy occurred in 9 Mean composite cognitive score was Conclusions : Hyperhomocysteinemia is associated with cognitive impairment in Nigerians with PD seen at the Lagos University Teaching Hospital as previously documented from other populations.

    Background : Parkinson's disease PD is a neurodegenerative disorder diagnosed clinically based on the signs of resting tremor, bradykinesia, rigidity and loss of postural reflexes. Here, we identify an excitatory circuit within the AOB network that entrains oscillatory activity in a second MC subpopulation. Using a battery of physiological techniques in acute AOB tissue slices, we investigate the physiological mechanisms underlying entrained oscillatory discharge.

    Entrained MCs display periodically increased excitatory synaptic input that correlates with rhythmic discharge patterns. Block of fast glutamatergic synaptic transmission reveals that a neural entrainment depends on an intact glutamatergic network, and b excitation reinforces burst intensity and increases precision in intrinsically oscillating MCs.

    Ongoing experiments aim to unravel the network mechanisms underlying MC entrainment and the role of slow rhythmic burst activity in AOB sensory information processing. Inhibitory circuits are a hallmark of computation in the brain. In the olfactory system, we have recently shown that inhibition in the mouse olfactory bulb OB is involved in odour fine discrimination behaviour. Optogenetic silencing experiments in anaesthetized and passive awake mice have suggested that distinct interneuron circuits fulfil specific roles in the OB, namely that superficial interneurons shape slow temporal features while deep interneurons, most notably including granule cells GCs , orchestrate activity across the OB on faster timescales.

    Surprisingly, silencing GCs in the anaesthetized preparation had essentially no impact on baseline activity of projection neurons both in anaesthetized and awake animals. Moreover, GC themselves were virtually silent largely less than 1 Hz baseline firing in both anaesthetized and passive awake mice. Here I will discuss these results and compare the contribution of inhibitory circuits in anaesthetized, passive awake and behaving mice using cell-specific optogenetic silencing, imaging and whole-cell recordings in head-fixed preparations. The ability to respond to chemical signals from the environment is essential for the survival and procreation of most organisms.

    Olfactory behavior represents an important substrate for adaptive evolution, as evident from the rapid evolution and diversification of chemoreceptor families. Evolution acts on genetic variation within a population. Thus, an assessment of the genetic underpinnings that give rise to natural variation in olfactory perception is critical for understanding the relationship between evolution of olfactory systems and environmental adaptation.

    Insect systems are ideal for formulating fundamental concepts of evolutionary adaptation of olfactory behavior, because they are highly amenable to integrative interdisciplinary strategies that combine ecological studies, genetic analyses, behavioral assays, and neuroanatomical approaches. This symposium will showcase studies to explore natural variation, evolution and adaptation in insect olfactory systems.

    Speakers will present genetics of variation and adaptation of Drosophila to host plants, the ecological significance of discrete olfactory pathways in flies, adaptive evolution of gustatory responses in cockroaches, and genetic studies on moths that give insights into the coevolution of diversification of pheromone blends and concomitant adaptations of partners responding to these blends, including the identification of genes that mediate such adaptation. Participation in the symposium by Dr. Katsumata is made possible through support from the W.

    Most night-flying moth species locate mates through production of, and response to, a very precise blend of volatile chemical compounds. Within a population, females with atypical blends are less attractive to males than females with the common blend. Similarly, rare males that respond to atypical blends are at a disadvantage in finding mates.

    This type of sexual communication system is expected to be evolutionarily constrained by stabilizing selection. Therefore, it is difficult to account for the great diversification of pheromone blends used by over , moth species. Genetic, physiological, and ecological studies will be discussed that give insights into the coevolution of diversification of female pheromone blends and concomitant adaptations of male partners responding to these blends, including the identification of genes that mediate such adaptation. Chemoreception is a principle sensory modality by which many organisms gain information from, and survive in, their environment.

    Variation in responses to the chemical environment, such as the olfactory preferences of insects for their host plants, may result in differential reproductive fitness, and shifts in preference may lead to divergence in host-adaptive traits, and ultimately result in reproductive isolation among populations. Here we examine differences in the genetic and neuronal underpinnings of the olfactory system between populations of the cactophilic fly, Drosophila mojavensis.

    This fly feeds and breeds on cacti in arid regions of Baja and the deserts of Mexico and the southwestern U. Four geographically distinct populations exploit four different cactus species that emit specific combinations of volatiles that serve as primary cues for host plant identification. Data show divergence between the populations in olfactory electrophysiology, behavioral preferences to cactus volatiles, and in the chemosensory transcriptome. Department of Entomology and W. In response to the anthropogenic assault of toxic baits, populations of the German cockroach have rapidly evolved a novel adaptive behavior a behavioral aversion of glucose, a phagostimulant component of baits that lets cockroaches avoid the bait.

    To understand the mechanisms of glucose aversion, we compared the electrophysiological responses of gustatory receptor neurons GRNs of the mouthparts to glucose, fructose and caffeine between wild-type and glucose-averse cockroaches. In both strains, the phagostimulant fructose stimulated a sugar-GRN, whereas caffeine, a bitter deterrent compound, stimulated a bitter-GRN.

    Glucose, like fructose, also simulated the sugar-GRN in wild-type cockroaches, but in glucose-averse cockroaches it stimulated both sugar- and bitter-GRNs. The results suggested that an acquisition of sensitivity for glucose in bitter-GRNs is responsible for glucose-aversion behavior. Moreover, we hypothesized that the native glucose-GRs, which should be expressed only on sugar-GRNs, are also misexpressed on the bitter-GRN in glucose-averse cockroaches, and carried out chemical structure-GRN activity experiments with glucose and three related compounds.

    We suggest that in glucose-averse cockroaches the expression of a broadly tuned receptor or multiple narrowly tuned receptors may contribute to the broad acceptance of glucose and related compounds by the bitter-GRN, driving aversive behavior. In the past 15 years, the fundamental molecular and neuronal logic of peripheral olfactory coding in the vinegar fly, Drosophila melanogaster has been largely deciphered.

    The next major challenge is now to identify how the olfactory system fits the ecological needs of the organism. I will here outline recent work from our lab aiming at unraveling the ecological significance of discrete olfactory pathways in the fly. These talks will begin to integrate our current understanding of these phenomena across experimental approaches from human psychophysics to fMRI to rodent neurophysiology.

    Because cognitive factors may be particularly important in taste and smell in comparison to vision or audition , this session will discuss them as a shared challenge for all chemosensory researchers. John McGann will briefly introduce the problem of cognitive influences on chemosensation, including traditional psychological perspectives e. Bayesian probabilistic networks, mutual information. This leads to the main question of the symposium: How does the brain actually implement these cognitive effects on chemosensation?

    This question will be addressed in four talks: 1 Dana Small on how expectations can influence taste perception and gustatory cortical activity in human subjects, 2 Wen Li on how emotion, anxiety, and threat perception can influence olfactory perception and brain physiology in human subjects, 3 Anan Moran on changes in the neural representations of tastants in the rat gustatory cortex as the behavioral significance of the tastant changes, and 4 John McGann on how expectation can influence neurophysiological responses to odors in the mouse olfactory bulb.

    Acknowledgements: Support indicated for each talk individually. Perceptual experiences result when physiochemical stimuli are transduced into nerve impulses and then elaborated and integrated in the central nervous system to inform ongoing behavior. In prior work we have shown that the canonical attention network upregulates insular response during directed attention to taste and breaches of taste expectation presumably to support orientation, identification, and learning about salient stimuli.

    More recently, we have uncovered evidence that this same network supports more prolonged benefits to taste sensitivity. This effect is replicated across four days, but the change in sensitivity is transient, with intensity ratings equivalent to the day 1 baseline at the start of each day. We also found that the effect is equal for all the taste stimuli, supporting a central, rather than a peripheral mechanism.

    A subsequent fMRI study confirmed this hypothesis showing enhanced insular responses to taste following the discrimination task e. Connectivity analyses then identified a pathway of information flow from the canonical attention network intraparietal sulcus and frontal eye fields to the amygdala and finally insular cortex.

    This suggests that, in addition to acute modulation, the canonical attention network may produce prolonged effects on gustatory cortex via an amygdala-mediated mechanism. Phylogenetically the most ancient sense, olfaction ties closely with primitive needs related to homeostasis and emotion, and changes in these internal states can greatly impact olfactory processing and experience.

    However, mechanisms underlying such state-dependent olfactory processes remain unclear. Perturbing the internal state with anxiety induction in human subjects, we interrogated emotion-state-dependent olfactory processing in a functional magnetic resonance imaging fMRI study. Following anxiety induction, initially neutral odors became unpleasant and took longer to detect, accompanied by augmented response to these odors in the olfactory anterior piriform and orbitofrontal cortices and emotion-relevant pregenual anterior cingulate cortex. In parallel, the olfactory sensory relay adapted with increased anxiety, incorporating amygdala as an integral step via strengthened afferent or efferent connections between amygdala and all levels of the olfactory cortical hierarchy.

    This anxiety-state-dependent neural circuitry thus enabled infusion of limbic affective information throughout the olfactory sensory progression, driving affectively charged olfactory perception. These findings could constitute an olfactory etiology model of emotional disorders, as exaggerated emotion-olfaction interaction in negative mood states turns innocuous odors aversive, fueling anxiety and depression with rising ambient sensory stress. Gustatory cortical GC neurons encode information relevant to behavior: information that should change as that behavior changes with learning, for example when a palatable taste becomes aversive and elicits rejection behavior rather than consumption.

    The observed relation between the mutual changes in the neural responses and behavior, although theorized to be of a causation nature, might be misleading, and cannot be validated in simple learning studies which may simply show neuronal response changes with experience. Neural activity that truly tracks behavior as opposed to simply changing with experience will not only change with learning but also change back when that learning is extinguished.

    To probe for this pattern we recorded the activity of ensembles of GC single neurons as rats that normally consumed sucrose avidly were trained first to reject it i. In contrast, using hidden Markov models HMM to probe for ensemble dynamic activity we have found that these dynamics actually followed the behavior pattern, changing with learning and reverting with extinction. Specifically, we have found that both the speed of ensemble-level taste processing and the relationships among ensemble responses to the different stimuli tracked behavioral relevance. These data suggest that population coding is linked to behavior with a fidelity that single-neuron coding is not.

    John P. This knowledge can include the relative frequency that odors are encountered in the environment, the significance of olfactory stimuli, and the relationships between odors and other sensory stimuli. By using this knowledge, the olfactory system can potentially adapt to different behavioral or sensory circumstances by incorporating expectations into its analysis of ongoing sensory input. This talk will present neurophysiological evidence that each of these types of information is incorporated into olfactory processing as early as the olfactory sensory neurons OSNs themselves.

    Several labs have now demonstrated that odor exposure induces odor-specific plasticity in the behavior of OSNs as the system adapts to the changing natural statistics of the olfactory environment. We have also shown that the OSNs become selectively hyper-responsive to odorants that predict an impending footshock after fear learning. Using optical neurophysiological techniques in gene-targeted mice, we have found that certain expectation violations induce a burst of activity in GABAergic interneurons that suppresses the synaptic output of OSNs via GABA B receptor-mediated presynaptic inhibition.

    This incorporation of stimulus contingency information into peripheral sensory processing is unexpected and may help to relate sensory processing to higher-level cognitive functions like attention and memory retrieval. Given the rising incidence and complications attributed to obesity and metabolic disorders, the purpose of the presidential symposium is to highlight the impact of obesity on the physiological processes of brain and sensory function.

    He will describe his electrophysiological and behavioral work on integration of nutrient information in the brain using widely-projecting hypothalamic circuits as a model. Sensory physiology experts will then present their findings of how excess energy perturbs the sensory modalities in terms of function or structure. Tim Kern Case Western Reserve will address how hyperglycemia causes diabetic retinopathy and his current research strategies designed to prevent this disease, Robin Dando Cornell University will discuss inflammation and cell cycle disruption of taste cells following diet-induced obesity, Nicolas Thiebaud The Florida State University will present data demonstrating sustained problems attributed to diet-induced obesity on olfactory structure and function, and Claire Murphy San Diego State University will present data on humans that demonstrate changed fMRI activity correlated to BMI in response to odor stimulation.

    Neurons whose activity is regulated by glucose are widespread throughout the brain. Glucose-excited GE neurons increase while glucose-inhibited GI neurons decrease their action potential frequency as extracellular brain glucose levels increase. We hypothesize that these neurons evolved to sense and respond to severe energy deficit e. We have shown that their response to falling glucose levels is enhanced during energy deficit. While this would be beneficial during times of famine, it would also reinforce the drive for compensatory feeding after voluntary weight loss. Consistent with this hypothesis, we find that activation of lateral hypothalamic orexin neurons in low glucose enhances excitatory drive onto downstream reward neurocircuitry.

    This lecture will discuss the mechanisms by which glucose sensing neurons sense changes in extracellular glucose and explore the roles of these specialized glucose sensors in glucose and energy homeostasis. Particular emphasis will be paid to the potential of lateral hypothalamic orexin glucose-inhibited neurons to induce persistent changes in glutamate signaling onto ventral tegmental dopamine neurons under conditions of glucose and energy deficit.

    These data support the hypothesis that altered glucose sensing in orexin neurons contributes to weight regain after dieting as well as binge-eating disorders by enhancing the reward value of food. Diabetic retinopathy is a major cause of vision loss in adults, and includes both a local vascular and neural disease. Using selective pharmacologic inhibitors or genetically modified animals, an increasing number of therapeutic approaches have been identified in animals that significantly inhibit the development of the diabetes-induced degeneration of retinal capillaries.

    A common feature of these approaches is that they inhibit production of oxidative stress or inflammatory mediators. Inhibition of the oxidative stress, which comes from both NADPH oxidase and mitochondria, inhibits the local induction of inflammatory molecules, suggesting that the oxidative stress is upstream of the induction of inflammatory molecules. Leukocytes play a critical role in oxidative stress, inflammation and development of vascular pathology, because deletion or blocking the interaction of leukocytes with endothelial adhesion molecules, or deleting proinflammatory signaling selectively within the leukocytes inhibits the diabetes-induced induction of oxidative stress, inflammatory molecules and degeneration of retinal capillaries.

    Recent evidence demonstrates that the diabetes-induced oxidative stress that develops in the retina is generated largely in a specialized sensory neuron, the retinal photoreceptors, and deletion of retinal photoreceptors or slowing of the visual cycle inhibits both the oxidative stress and the local inflammation in the retina.

    These hypotheses offer novel targets at which the microvascular disease might be inhibited, but therapies that inhibit the vascular disease do not necessarily correct the diabetes-induced dysfunction of retinal neurons vision. Obesity is a powerful inflammatory state, governed primarily by the foods we eat. Despite our knowledge of nutrition being higher than at any point in history, we still select our foods primarily by their hedonic properties, we eat the foods that taste good.

    For many years, human psychophysical studies have reported lower sensitivity to tastes in the obese. There has however, been some disagreement over cause and effect, whether those born with a weak sense of taste are more likely to become obese, or becoming obesity weakens a healthy sense of taste.

    Recently, my lab has examined the molecular effects of obesity on the taste bud. Mice fed a regimen high in dietary fats HFD for only a few weeks rapidly become obese, and interestingly have significantly fewer taste buds assayed via immunohistochemical cell-counting than littermates fed standard lab chow. In a state of obesity, many inflammatory markers are elevated, leading to a number of well-documented pathological consequences.

    HFD-fed mice exhibit prominent apoptosis measured with TUNEL staining in taste buds and taste stem cells, with vastly elevated markers for the extrinsic apoptosis pathway. These results would allude to the presence of an obesogenic feedback loop within the taste bud, with consumption of more tasteful, calorie-dense foods resulting in a lower ability to taste such stimuli, thus driving higher consumption.

    Nicolas Thiebaud 1 , Genevieve A. Bell 1 , Kassandra L. Ferguson 1 , Erminia Fardone 1 , Melissa A. Cooper 1 , Arda B. Celen 1 , James A. Warrington 1 , Debra Ann Fadool 1,2. Energy homeostasis is achieved through a coordinated regulation between the peripheral organs and the brain. We quantified loss of olfactory sensory neurons and their axonal projections after exposure to a fatty diet, with an associated reduction in electroolfactogram amplitude. Loss of olfactory neurons and associated circuitry was linked to changes in neuronal proliferation and normal apoptotic cycles.

    By placing obesity-prone mice on high-fat diets upon weaning and at middle age we were able to stimulate mice with odors and assess a reduction in immediate early gene activation following sustained consumption of fatty diets. Using a computer-controlled, liquid-based olfactometer, mice maintained on fatty diets learned reward-reinforced behaviors more slowly, had deficits in reversal learning demonstrating behavioral inflexibility, and exhibited reduced olfactory discrimination.

    When obese mice were removed from their high-fat diet to regain normal body weight and fasting glucose, olfactory dysfunctions and concomitant anatomical losses were retained. We conclude that chronic energy imbalance therefore presents long-lasting structural and functional changes in the operation of the sensory system designed to encode external and internal chemical information and leads to altered olfactory- and reward-driven behaviors.

    Obesity has reached epidemic proportions, motivating research into the underlying mechanisms driving obesity and its consequences. Olfaction is a powerful motivator for food consumption. Research in animal models suggests that metabolic status and hormones involved in satiety may play critical roles in modulating olfactory sensitivity. In rodents olfactory sensitivity is increased during the hunger state and decreased in satiety.

    Rodents fed a high fat diet show electrophysiological responses that indicate decreased sensitivity to odor. In humans, event-related potentials indicate slowed brain response as BMI increases in older adults. Neuroimaging of the human brain demonstrates differences in response to taste in gustatory and reward areas during hunger and satiety. Here we consider the response to odor in brain regions of interest for olfaction, reward and memory in participants tested under the conditions of hunger and satiety.

    We used functional MRI to scan at 3T in a GE excite scanner while participants provided modified gLMS ratings of the pleasantness of citral, a food related odor presented orally, under conditions that mimic natural flavor perception. Overall, response to odor was greater in the hunger than in the sated state. Responses in reward related brain areas decreased with increasing BMI, indicative of a blunted reward response, which was especially prominent in the hunger condition. Results support modulation of central response to odor in humans by metabolic state. We gratefully acknowledge the assistance of the members of the Lifespan Human Sense Laboratory.

    We thank Dr. Jennifer Beshel, Yi Zhong. Motivated feeding results from the interplay of homeostatic and hedonic drives and dysregulation of either may contribute adversely to conditions of overweight and obesity. Interestingly, knockdown of endogenous domeless-ligand upd2 in the fat body of flies leads to smaller body size and has no effect on feeding, the opposite behavior of leptin-deficient mammals. While we replicate the lower weight and unchanged food intake in upd2-manipulated flies, we further show manipulations to another endogenous ligand for the domeless receptor, brain-based unpaired 1 upd1 , recapitulate mammalian obesity phenotypes in flies.

    Flies with reductions in upd1 restricted to neural tissue show increased weights, increased food intake, and increased attraction to food odors. We additionally report domeless receptors likely mediate observed phenotypes. We show behavior-relevant domeless receptors are located on neurons expressing Drosophila Neuropeptide F dNPF , the Neuropeptide Y NPY homolog, in the central brain with targeted receptor knockdown specifically to these cells replicating increased weight, attraction and intake phenotypes.

    We speculate upd1 acts as the homeostatic regulator of our previously reported dNPF food odor value signal, up- or down-regulating this hedonic signal as a function of satiety state. Our findings suggest Leptin-NPY and upd1-dNPF represent functionally homologous circuits across diverse species and imply in mammals adipose- and less understood brain-derived Leptin may play different roles in feeding and weight regulation. Shipley 2 ,. Serotonergic inputs from the raphe nuclei innervate all layers of the olfactory bulb OB , yet the effects of serotonergic modulation on OB circuits remain unclear.

    Here, we examine how raphe projections modulate OB inter- and output neuron activity in vivo. First, we tested whether raphe stimulation affected juxtaglomerular interneuron activity by imaging calcium transients from periglomerular PG or short axon SA cells expressing GCaMP. We next expressed the genetically-encoded reporter of glutamate transmission iGluSnFR in PG or SA cells and observed a similar enhancement of inhalation-evoked glutamate transients in each cell type, suggesting that raphe inputs increase sensory-driven excitation onto PG and SA cells. Consistent with this, optogenetically activating serotonergic projections from raphe during extracellular recording of putative MT cells led to a tonic increase in MT cell firing rate without altering inhalation-driven transients.

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    Together, these results demonstrate a differential effect of serotonergic modulation on interneurons and output neurons in the OB and point to glutamatergic juxtaglomerular neurons — such as external tufted cells - as a key target of serotonergic modulation from the raphe. Archana Kumari 1 , Alexandre N. Ermilov 2 , Libo Li 1 , Benjamin L. Allen 3 , Robert M. Bradley 1 , Andrzej A. Dlugosz 2,3 , Charlotte M. Mistretta 1.

    However, HPI treatment results in severe taste disturbances. Strikingly, we had shown that 16 days of LDE gavage caused disruptions in taste organs and taste sensation, while 28 days of treatment eliminated normal taste organs and taste responses. Papillae, taste buds and taste cell types were quantified. Importantly, we observed recovery from these effects within 14—21 days after discontinued HPI treatment. Further, conditional genetic disruption of SMO in the lingual epithelium resulted in similar alterations in taste organ morphology.

    Remaining taste bud cells in HPI-treated or SMO mutant mice expressed the taste cell marker K8 and there was retained innervation to papillae and apical epithelium seen with neurofilament and P2X3 antibodies. All taste bud cell types were reduced progressively over treatment days. These data identify a requirement for HH signaling in maintaining papilla and taste bud integrity, and strongly support the concept that taste disturbances in LDEtreated patients reflect a direct response to HH pathway inhibition in human taste organs.

    Taste and smell are intimately connected, as evidenced by the multisensory nature of our sense of flavor. Psychophysical studies on odor intensity perception in humans, as well as behavioral work on odor preference and aversion learning in rodents have suggested that taste influences smell. By combining multi-site electrophysiology and optogenetics in behaving rats, we demonstrate that the gustatory system modulates the olfactory system via interactions at the level of primary sensory cortex.

    We recently identified neurons in the piriform cortex PC of rats that receive taste-selective input, and form functional interactions with neurons in primary gustatory cortex GC : optogenetic inhibition of GC GCx during taste processing eliminates taste-selective responses from PC. Increases and decreases in firing rate were observed equally likely, effectively changing the neural ensemble activated by a given odorant.

    Next, we probed the possible effect of altered odor representation during GCx on odor perception in a unimodal olfactory learning task. Rats were conditioned to prefer a novel, previously neutral odor by associating that odor with a reward. GCx during subsequent preference testing revealed that rats were unable to express this learnt preference, suggesting that GCx changes the way an odor is perceived. Thus, we demonstrate an unexpected consequence of intrinsic functional connectivity between the taste and smell systems.

    Correlating olfactory receptor OR activation patterns with human odor perception is a challenge due to the combinatorial nature of the olfactory code and our limited knowledge of odor ligands for these receptors. By examining cases in which loss-of-function of a single OR has a significant role in odor perception, we can begin to determine the conditions in which in vitro OR function predicts human behavior. We then set out to identify the causal receptor underlying each association using an in vitro assay.

    For these ORs, human behavior, in particular perceived intensity, correlates with in vitro receptor function. However, using in vitro receptor function to predict human behavior is less clear. In vitro OR function strongly predicts perceived odor intensity for high affinity odor ligands, but poorly for low-affinity ligands. Cilia dysfunction underlies a class of human diseases with variable penetrance in different organ systems.

    Across eukaryotes, intraflagellar transport IFT facilitates construction of olfactory sensory cilia and ciliary cargo trafficking, thereby enabling olfaction, but our understanding of mammalian IFT is insufficient. Here we perform live analysis of cilia ultrastructure, composition and cargo transport dynamics in native mammalian olfactory sensory neurons using Total Internal Reflection Fluorescence microscopy TIRFm.

    Proximal and distal axonemes of these neurons show no bias towards IFT kinesin-2 choice, and Kif17 homodimer is dispensable for distal segment IFT. Our results yield a model for IFT and cargo trafficking in native mammalian cilia and may explain the penetrance of specific ciliopathy phenotypes in olfactory neurons. Acknowledgements: R01DC to J. T32DC to C. It has been argued that birds have a lower taste acuity compared to mammals due to their low taste bud numbers. In addition, chicken seem have fewer taste receptor genes: the sweet taste receptor is missing and their bitter taste receptor repertoire is very small, consisting of only three members.

    However, knowledge emerging from genomes sequencing suggests that birds have a well-developed taste system which differs significantly among different species. Behavioral and genetic evidence show that birds have an accurate capacity to detect different taste modalities. In fact, the bitter taste reception in chicken is a minimalistic model for studying bitter taste, which is much more complex in human 25 receptors and mice 30 receptors.

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    Furthermore, birds present a unique opportunity to study taste evolution in different ecological niches. The symposium features recent contributions from several researchers. In particular, Dr. Behrens will present results on chicken bitter taste receptors repertoire, in comparison with bitter taste receptors in other species. Masha Niv will present studies on molecular recognition of bitter tastants, focusing on issues of selectivity and promiscuity of both ligands and receptors. Finally, Maude Baldwin will present the study on the repurposing of an amino acid taste receptor to respond to sugars and other sweeteners in the hummingbird.

    The symposium is aimed at audience interested in evolution, molecular recognition, taste programming and farm animal nutrition. Nutritional chemosensing has gained momentum thanks to the discovery of a broad array of nutrient sensors, including taste receptors Tas1r and Tas2r , most of them known to be expressed in the oral cavity in mammals. Compared to mammals taste in birds has been regarded to be less developed because they seem to have a low number of taste buds, lack the Tas1r2 and have only few bitter taste receptors. The aim of our research is to evaluate the nutrient sensing system in birds using the domestic chicken as a model.

    We have measured the size of the oral cavity with the hypothesis that the number of taste buds is proportioned to the oral volume with a similar ratio in birds and mammals. Thirty-three oral cavity plaster moulds were constructed from chicken heads. We found that the average oral volume of a chicken was 2. We conclude that chickens have a well-developed nutrient sensory system. Our results set the scene for future studies in chickens related to taste and nutrient appetites.

    Acknowledgements: The research has been partially covered by the University of Queensland post-doctoral fellowship scheme. Maik Behrens 1 , Sigrun I. Korsching 2 , Wolfgang Meyerhof 1. The detection and avoidance of potentially harmful bitter food compounds is important for the survival of animals. Recognition of bitter substances is facilitated by bitter taste receptors located in the oral cavity. The number of functional bitter taste receptor genes deviates considerably among animal species ranging from very few to more than Although it has been hypothesized that birds may possess inferior tasting abilities due to low salivation, a lack of mastication and a low number of taste buds in their oral cavity, all bird species investigated so far possess small to mid-sized Tas2r gene repertoires.

    This raised the question of whether the sizes of avian Tas2r gene repertoires correlate with the relative importance of the bitter tasting abilities of bird species, or whether such predictions are not possible. In order to determine the recognition profiles of avian Tas2rs we cloned bitter taste receptor cDNAs of two phasianid G.

    After screening of the receptors with 46 mostly natural bitter compounds, the responding receptors were further analyzed with the activating bitter substances to determine more detailed response characteristics. We found that all of the chicken and turkey receptors exhibit broad tuning properties suggesting that small Tas2r gene repertoires do not necessarily indicate inferior bitter compound detection.

    An expansion of the Tas2r gene number in zebra finch, however, seems to allow the development of more specialized bitter taste receptors. Our results show that the investigated bird species are well equipped for the detection of potentially harmful bitter substances, a finding that agrees well with behavioral data obtained for chicken. Maude W. Klasing 4 , Takumi Misaka 2 , Scott V. Edwards 1 , Stephen D.

    Liberles 5. In addition, chemosensory receptors represent a direct link between genotype and phenotype and yield insight into basic aspects of the evolutionary process. In mammals, sweet taste perception is mediated by a G protein-coupled receptor complex; however, the gene encoding one subunit of the mammalian sweet receptor T1R2 has not been detected in any bird genome, suggesting loss in the avian common ancestor. Nevertheless, many nectar-feeding birds, such as hummingbirds, lorikeets, and honeyeaters display high behavioral affinity for sugars found in nectar.

    To understand the molecular basis of sugar sensing in hummingbirds, we cloned members of the T1R taste receptor gene family from oral tissue of hummingbirds, swifts, and chickens. Receptor expression studies revealed that the ancestral umami receptor T1R1-T1R3 heterodimer was re-purposed in hummingbirds, but not in swifts, their closest relatives, to function as a carbohydrate receptor. Behavioral choice tests and high-speed videography in wild and captive hummingbird populations indicated sweet taste preferences that correlated with in vitro functional studies.

    This change in taste receptor function may have been one of many key adaptations enabling hummingbirds to detect and utilize nectar, facilitating the radiation of hummingbird species. Bitter compounds are numerous and chemically diverse 1. These compounds are recognized by one or more GPCRs from the T2Rs subfamily, which, in turn, may recognize either few or numerous ligands 2. Iterative homology modeling, docking, and site-directed mutagenesis suggest that common strategies enabling T2Rs to recognize diverse ligands include ligand-specific engagement of different sets of partially overlapping positions within the same binding pocket, and employment of different types of interactions by the same residues 3.

    Analysis of experimental GPCR structures highlights hydrophobicity and binding site exposure as general features predictive of the levels of promiscuity of GPCRs 4. A ligand promiscuity predictor was developed for identifying bitter ligands that activate multiple T2Rs. The molecular determinants responsible for activity and selectivity of bitter compounds for chicken bitter receptors were investigated by ligand-based and structure-based methods. Identification of novel T2R-selective and T2R-promiscuous bitter ligands for chicken and for human is currently underway. Wiener, A. Nucleic Acids Res ,.

    Di Pizio, A. Isr J of Chem, special issue Born, S. J Neurosci , 33 1 , — Levit, A. J Chem Inf Model , 54 1 , — As is true in all sensory systems, chemosensory perception reflects not only the external stimulus, but also the internal state and past experiences of the perceiver. That is, the same basic sensory circuit may produce different outputs depending on internal state and past experience.

    These changes in sensory coding and circuit function appear to derive from changes in both neuromodulatory tone and from feedback from higher order, non-sensory circuits. While these processes occur in all sensory systems, they may be particularly relevant in the chemical senses which monitor stimuli relevant to nutrition, reproduction, kin recognition and predator avoidance. This symposium will present new data from both the olfactory Kay, Mandairon, Sadrian and gustatory Fontanini systems exploring how this internal modulation occurs.

    The talks will include diverse research techniques primarily in awake animals e. Discrimination learning through experience serves as the basis for adaptive behavior thanks to structural and functional changes in the brain. In the olfactory system, two main forms of experience, perceptual and associative learning have been show to modulate discrimination and neural activity in the olfactory bulb.

    This cortical structure is the first central relay of olfactory processing and the target of adult neurogenesis. The olfactory bulb is in fact capable of generating new neurons that can integrate into its complex circuitry. Both associative and perceptual learning have been shown to increase neurogenesis but while perceptual learning requires neurogenesis as soon as its acquisition, associative learning needs it to maintain memory suggesting different role of adult-born neurons in learning processes and thus different mechanisms underlying their integration into the bulbar network.

    It is well known that centrifugal inputs to the olfactory bulb and more specifically noradrenergic and cholinergic systems contribute to learning processes. We will discuss how these neuromodulatory systems may differentially interact with neurogenesis to allow perceptual and associative learning processes. Leslie M. Kay 1,3 , Donald E. Frederick 1,3 , Boleslaw Osinski 2,3. These oscillations are not just different frequencies but appear to rely on different circuits. Gamma oscillations increase in amplitude when central input to the OB is silenced; beta oscillations are ablated in this condition.

    Gamma oscillations are enhanced during fine odor discrimination, while beta oscillations are not. We tested the task requirements of these two oscillations by training separate groups of rats on each task in parallel. We found that both tasks produce both types of oscillations, but gamma and beta represent different parts of the discrimination process. Gamma oscillations dominate the first 2—3 sniffs of the odor, while beta oscillations correlate with the end of odor sampling and preparation for a learned response.

    Beta oscillation power also depends on the odors being sampled. During fine odor discrimination gamma oscillations are enhanced and beta oscillations are increased before and decreased during odor sampling. These results show that the early olfactory system can occupy several different functional states within an odor sampling bout and across tasks and odor sets.

    Computational modeling indicates that changing the state of OB granule cells can transition the system from gamma to beta modes. These states are likely determined by the cognitive context of the behavioral task, which is associated with dynamics in neuromodulatory tone and centrifugal input to the OB. The rodent piriform cortex PCX is a paleocortical structure known to support olfactory perception toward learned behavior. While the anterior PCX is used in associative odor object information decoding, the posterior PCX receives more descending input fibers from brain structures such as the amygdala that are thought to provide a qualitative relevance to raw odor percepts.

    Here we investigate the influence of top-down influence of specific brain regions on spontaneous and odor-induced activity in the posterior PCX at the single unit level. Using optogenetic techniques, we artificially stimulated descending fibers in the posterior PCX that were virally transduced from one of two interconnected brain regions. Photostimulation at nm and 1mW near infected axon terminals in the posterior piriform was sufficient to drive temporally coincident responses of unit activity and local field potential, as recorded in anaesthetized animals injected at any one of the two target regions.

    Odor-paired photostimulation of descending fibers at the posterior PCX modulated local single unit response patterns compared to odor only. Photo-induced effects on unit odor responses ranged from suppressive to stimulatory, which often varied depending on the combinatorial timing of odor and light stimulation. These results demonstrate the importance of top-down inputs to piriform cortex in odor coding, and highlight that cortical odor processing takes place in a rich milieu of sensory, emotional and contextual information. Acknowledgements: DC AA The gustatory cortex GC of alert animals does much more than process the physiochemical properties of taste.

    Besides flexibly representing the chemosensory information, GC neurons also encode hedonic value and expectation of taste. Over the past years, our group has focused on understanding how GC represents anticipatory information. I will present recordings from the GC of alert rodents showing that neurons respond to cues that anticipate the general availability of taste and cues that predict specific tastants. Cue responses develop with learning and can be triggered by stimuli belonging to multiple sensory modalities.

    I will present evidence of the involvement of anticipatory activity in modulating taste coding and feeding behaviors. In addition, I will discuss the role of thalamic and amygdalar inputs in mediating responses to anticipatory cues. These results challenge the idea of a clear separation between bottom-up and top-down channels of information. The presence of anticipatory signals in the VPMpc emphasizes how the integration of sensory and contextual signals is not just a cortical process, but can occur at any level of the gustatory system.

    On this bases, I will argue that current conceptualizations of the gustatory system as a pure labeled-line analyzer of chemical information need to be replaced by more complex models emphasizing context-dependency and integration. There is growing recognition that the cellular heterogeneity of the peripheral olfactory system is a major contributor to the complexity of olfactory function. Olfactory neurons can differ in their stimulus selectivity, transduction mechanisms, CNS targets and behavioral roles. This symposium will explore several cellular subpopulations in the olfactory periphery where cGMP signaling has been implicated, with a focus on their mechanisms for sensory transduction, their central targets, and their contributions to behavior.

    In his introduction, Steven Munger will provide a short history and important context for cGMP signaling in olfaction. Trese Leinders-Zufall will then discuss work from her and her colleagues dissecting the role of the Grueneberg ganglion and other olfactory subsystems in mediating aversive behaviors in the mouse. Joerg Fleischer will speak about studies in the Grueneberg ganglion from his group that dissect the mechanisms of chemo- and thermosensation in this still obscure sensory organ.

    Finally, Peter Mombaerts will discuss his recent work on a novel subpopulation of mouse MOE neurons that express both Trpc2 and cyclic nucleotide-gated channels, some of which express a soluble guanylyl cyclase. Together, the speakers will provide a new understanding of the importance of heterogeneous signaling mechanisms in the olfactory system across multiple species and will suggest implications for olfactory functions.

    Elissa A. Hallem, Manon L. Guillermin, Mayra A. Castelletto, Spencer S. Carbon dioxide CO 2 is a critical sensory cue for many animals that can signal the presence of food, mates, predators, or hosts. We are investigating the neural basis of CO 2 sensing in the free-living nematode C. We have found that C. A network of interneurons mediates CO 2 response, and behavioral sensitivity is modulated by opposing interneurons.

    Like C. Moreover, CO 2 is an essential host cue for EPNs: attraction to insect odor is greatly decreased or eliminated when CO 2 is chemically removed. The passively ingested livestock parasite Haemonchus contortus is also attracted to CO 2 , a behavior that may increase the likelihood of passive ingestion.

    By contrast, skin-penetrating nematodes, including the human threadworm Strongyloides stercoralis , are repelled by CO 2. However, skin-penetrating infective larvae require CO 2 for development inside the host, indicating that CO 2 is a critical developmental cue for these parasites. The BAG neurons of S. We are now testing the hypothesis that cGMP signaling by BAG neurons is required for skin-penetrating worms to infect hosts. Our results will provide insight into the role of cGMP signaling in mediating sensory behaviors, and may enable the development of new strategies for combating harmful nematode infections.

    Munger 2 , Frank Zufall 1 , Pablo Chamero 1. Detection of predators elicits stereotyped fear and innate evading responses on prey species. Preys frequently coexist with a large number of predator species, each emitting numerous distinctive chemical cues. The mouse olfactory system is composed of diversified subsystems that are distinguished by the signaling mechanisms they employ to transduce sensory stimuli and their axonal projections to specific regions of the olfactory forebrain.

    This organization enables the recognition of a broad range of chemicals, some of which activate developmentally programmed neural circuits eliciting avoidance. How olfactory signals are processed to exhibit innate avoidance remains largely unclear. We observe that mice display robust avoidance to specific odors released by predators. Mutant mice deficient for essential subsystem-specific signal transduction components fail to display innate avoidance responses to some predator odors while avoidance to odors detected by other subsystems remains unaltered.

    Predator odors are broadly detected by distributed populations of sensory neurons in the nose that innervate multiple glomeruli in the olfactory bulb, organized as independently initiated sensory circuits. We have begun to investigate the central brain areas that participate in the processing and integration of these olfactory signals to determine a circuit logic of innate kairomone avoidance. Acknowledgements: Supported by grants from the Deutsche Forschungsgemeinschaft to P.

    SFB and T. The Grueneberg ganglion - a cluster of neurons in the anterior nasal region — is considered as an olfactory subsystem that is activated by distinct odorants, in particular given pyrazine analogues. The odorant-responsive neurons are characterized by the expression of the guanylyl cyclase subtype GC-G and the cyclic nucleotide-gated ion channel CNGA3. The results of experiments with knockout mice disclosed that GC-G and CNGA3 are important for odor-evoked responses, suggesting a unique chemo-electrical transduction mechanism in the Grueneberg ganglion.

    Accordingly, the same subpopulation of neurons in the Grueneberg ganglion responds to both coolness and odorants. In search for temperature-responsive signaling proteins, it was found that the Grueneberg ganglion lacks the canonical cold receptor, the TRPM8 channel. Instead, the thermosensitive ion channel TREK-1 is expressed. However, it turned out that even in the absence of TREK-1, Grueneberg ganglion neurons were still activated by cool temperatures, leading to the notion that other coolness-responding molecular elements must exist.

    In this context, comprehensive biochemical analyses led to the unexpected finding that the guanylyl cyclase subtype GC-G is a very unusual enzyme which is directly activated by cool temperatures. In addition, the observation that Grueneberg ganglion neurons from GC-G-deficient mice showed a largely reduced responsiveness to coolness supports the concept that the guanylyl cyclase subtype GC-G may serve as a major thermosensor in neurons of the Grueneberg ganglion.

    Acknowledgements: This work was supported by the Deutsche Forschungsgemeinschaft. Chemoreception in the mouse olfactory system occurs primarily at two chemosensory epithelia in the nasal cavity: the main olfactory epithelium MOE and the vomeronasal epithelium VNE. The canonical chemosensory neurons in the MOE, the olfactory sensory neurons OSNs , express the odorant receptor OR gene repertoire, and depend on Adcy3 and Cnga2 for chemosensory signal transduction.

    The canonical chemosensory neurons in the VNE, the vomeronasal sensory neurons VSNs , express two unrelated vomeronasal receptor VR gene repertoires, and involve Trpc2 for chemosensory signal transduction. Recently we reported the discovery of two types of neurons in the mouse MOE that express Trcp2 in addition to Cnga2. These cell types can be distinguished at the single-cell level by expression of Adcy3: positive, type A; negative, type B. Some type A cells express OR genes. Among MOE cells, type B cells are unique in their expression of the soluble guanylate cyclase Gucy1b2.

    The generation of polyclonal antibodies against Gucy1b2 and a novel Gucy1b2-IRES- tauGFP gene-targeted strain enabled us to visualize coalescence of axons of type B cells into glomeruli in the main olfactory bulb. Acknowledgements: Max Planck Society. Chemical signals constitute an important medium for communication across a range of species, including humans, as recent evidence suggests.

    The type of information that can be communicated via chemical signals varies. For instance, mice have been shown to warn their conspecifics by sending alarm and disease signals. This symposium consists of four speakers whose work demonstrates that chemosignals of emotion and disease status constitute an important facet of social communication, not just in animals but also in humans. Lisa Stowers Scripps Research Institute will present data exploring the link between chemical communication and emotion in mice, and the opportunity for using molecular genetics for understanding the underlying mechanisms.

    Acknowledgements: R01MH While it is understood that mouse pheromones regulate social behavior, it is less well appreciated that these behaviors are tightly coupled with emotion. Emotional processing is one of the three major functions of the human brain along with sensory- and cognitive-processing. Inappropriate, exuberant or diminished display of emotion can be devastating. Even smart, logical and decisive individuals can suddenly become irrational, foolish, and reckless when emotion is strongly engaged. How can it be that almost nothing is known about the information processing and underlying mechanisms that generate emotion in any species?

    We are utilizing synthetic, emotion-generating pheromones provides an experimentally simple means to identify and study currently unknown subsets of relevant neurons that underlie the generation of emotion.