Abstracts - Association for Chemoreception Sciences

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#16 PRESIDENTIAL SYMPOSIUM: NEUROTRANSMITTERS AND NEUROMODULATORS IN THE TASTE BUD Modulation of sweet taste responses by orexigenic and anorexigenic factors Yuzo Ninomiya Section of Oral Neuroscience, Graduate School of Dental Sciences, Kyushu University Fukuoka, Japan Sweet taste perception is important for animals to detect external carbohydrate source of calories and has a critical role in the nutritional status of animals. Our previous studies demonstrated that the taste organ is a peripheral target for leptin, an anorexigenic mediator that reduces food intake by acting on hypothalamic receptors. In mice, increase in plasma levels of leptin leads to reduction of sweet taste responses of taste nerve and receptor cells via activation of leptin receptors. In human, the recognition thresholds for sweet compounds have a diurnal variation that parallels variation for leptin levels, with lowest in the morning and highest in the night. Plasma levels of leptin are shown to inversely correlate with circulating endocannabinonds (anandamide and 2-arachidonoyl glycerol), orexigenic mediators that induce appetite and stimulate food intake via CB1 receptors mainly in hypothalamus. Here, we investigated potential effect of endocannabinoids on sweet taste responses in mice and found that endocannabinoids oppose the action of leptin to act as enhancers of sweet taste. In wild type mice, administration of endocannabinoids enhances behavioral, taste nerve and taste cell responses to sweet taste without affecting responses to bitter, salty, sour and umami stimuli. In contrast, mice genetically lacking CB1 receptors show no such enhancement by endocannabinoids Endocannabinoids, therefore, not only stimulate food intake via central systems but also may increase palatability of foods by enhancing peripheral sweet taste responses. Reciprocal regulation of peripheral sweet taste reception by endocannabinoids and leptin may contribute to their opposing actions on food intake and play an important role in regulating energy homeostasis. #17 PRESIDENTIAL SYMPOSIUM: NEUROTRANSMITTERS AND NEUROMODULATORS IN THE TASTE BUD Insulin regulates the function of epithelial sodium channels and salt taste preference Timothy Gilbertson, Arian Baquero Department of Biology & The Center for Advanced Nutrition, Utah State University, Logan, UT USA Diabetes is a profound disease that is reflected in an impairment of systemic salt and water balance. We hypothesize that epithelial sodium channels (ENaC) in mouse taste receptor cells (TRCs) play a role in the restoration of salt and water balance by virtue of insulin’s effect on the taste system. In behavioral assays, insulintreated mice show avoidance of NaCl at lower concentrations than controls. These differences were abolished when amiloride was added into NaCl solutions suggesting that insulin was regulating ENaC. To test for the ability of insulin to alter ENaC function, we performed patch clamp recording on isolated mouse TRCs. In TRCs, insulin caused a significant increase in Na+ influx (EC50 = 6.1 nM). Similarly, using the Na-sensitive dye SBFI, increasing extracellular Na+ from 0 to 140 mM elicited an increase in Na+ influx in a subset of TRCs and insulin treatment (20 nM) enhanced this Na+ influx. To investigate whether ENaC function is altered during the onset of diabetes, we performed Na+ imaging in isolated TRCs from a mouse model of Type 1 diabetes. TRCs from diabetic mice exhibit amiloride-sensitive Na+ responses similar to non–diabetic littermates. However, insulin enhancement of Na+ influx via ENaC was abolished in diabetic TRCs. TRCs from diabetic mice exhibit greater responses to NaCl than those from non-diabetic mice and behaviorally diabetic mice showed avoidance of NaCl at significantly lower concentrations. In contrast, diabetic animals showed no significant avoidance to these NaCl solutions when amiloride was added to NaCl solutions indicating a role for ENaC in this increased sensitivity. Our results are consistent with the hypothesis that ENaC alterations during diabetes may be another example of the ability of the gustatory system to respond to nutritional challenges. Supported by NIH DC02507 (TAG). #18 SYMPOSIUM - CILIA, SENSORY DYSFUNCTION AND DISEASE Olfactory Cilia: Linking Sensory Cilia Function and Human Disease Jeffrey Martens University of Michigan Ann Arbor, MI, USA Cilia are intimately involved with the fundamental biological processes of photoreception, olfaction, and auditory function. The olfactory system is one of the multiple sensory systems that are critically dependent on the proper function of cilia. Non-motile sensory cilia on OSNs compartmentalize signaling molecules necessary for odor detection allowing for efficient and spatially confined responses to sensory stimuli. Since OSN cilia lack the necessary machinery for protein synthesis, nascent proteins must be transported from the cell body into the cilium. Movement along the ciliary axoneme is tightly regulated and involves evolutionarily-conserved intraflagellar transport (IFT) proteins. Joel Rosenbaum will discuss the basic mechanisms and regulation of IFT. Randall Reed and Jeffrey Martens will present work that elucidates specific mechanisms that are required for the translocation of the transductory machinery to the sensory cilia, as well as the human pathologies associated with defects in these processes. While it is clear that olfactory dysfunction is a clinical manifestation of a subset of ciliopathies, there appears to be a selective penetrance of phenotypes between different cilia in the body highlighting the necessity for comparison of multiple systems. Anand Swaroop will discuss mechanisms and clinical disorders associated with cilia dysfunction in the visual system while Kirk Mykytyn will talk about G-protein coupled receptor signaling in the CNS and its alteration in specific ciliopathies. Finally, Dominic Cosgrove will discuss the discovery of proteins that may link actin-based steriocilia of the inner ear to primary cilia. This session will highlight new cell biological approaches that can reveal not only mechanisms of fundamental olfactory processes. Acknowledgements: NIDCD (1R01DC009606-01) 12 | AChemS Abstracts 2010 Abstracts are printed as submitted by the author(s)
#19 SYMPOSIUM - CILIA, SENSORY DYSFUNCTION AND DISEASE Molecular Organization of Olfactory Transduction Components in Cilia Randall Reed, Abigail L. D. Tadenev, Adrian Cuenca Center for Sensory Biology, Johns Hopkins School of Medicine Baltimore, MD, USA Bardet-Biedl Syndrome (BBS) is a pleiotropic, heterogeneous disease associated with renal, mental, retinal, and early developmental anomalies. These phenotypes are consistent with defects in cilia formation or function. Identification of BBS8, one of 14 implicated in BBS, led to the hypothesis that BBS is caused by basal body and/or cilia defects. We previously showed that BBS patients and BBS mouse models exhibit impaired olfactory function consistent with the critical role of cilia in olfaction. We genetically ablated the mouse BBS8 gene since it is particularly abundant in OSNs and BBS8 antibodies reveal staining in dendritic knobs in a shell-like structure surrounding the basal bodies. BBS8 null mice have reduced olfactory responses by EOG recording. Immunofluorescence analyses of the OE reveal a dramatic truncation of OSN cilia, a disorganized dendritic microtubule network, and mislocalization of proteins normally enriched in cilia. Visualization of proteins in OSNs by genetic reporters reveals altered localization patterns. Although OSN numbers are largely normal, targeting of OSN axons to the olfactory bulb is aberrant; axons expressing the same receptor display reduced fasciculation and project to multiple targets. Using reagents that reveal the characteristic neuronal activity of each OSN, we observed altered activity in BBS8-null OSNs. We hypothesize that alterations in cilia structure, the essential signaling platform for olfaction, alters the uniformity of responses in populations of OSNs expressing the same OR. In parallel, we have examined the requirements for specific olfactory transduction components to localize to cilia in cell-culture systems. This has led to valuable new tools to evaluate the mechanisms of cilia enrichment and dynamic properties of these sub-cellular structures. Acknowledgements: This work was supported by NIH grant DC04553 #20 SYMPOSIUM - CILIA, SENSORY DYSFUNCTION AND DISEASE Intraflagellar Transport functions in cilia assembly and signalling processes, and also in exocytosis Joel Rosenbaum 1 , Cosima Baldari 2 , Francesca Fanetti 2 , Kaiyao Huang 1 , Chris Wood 1 1 Dept of Molecular, Cellular and Developmental Biology, Yale University , 2 Dept of Evolutionary Biology, University of Siena, Italy A major revival in research on cilia and flagella and their relationship to certain pathologies rested on the discovery of the IFT (Intraflagellar Transport) in all eukayrotic cilia and flagella, and the function of IFT in ciliary assembly and signalling processes. The cloning of the IFT genes led, first, to the ciliary hypothesis of PKD (Polycystic Kidney Disease) and later to the discovery of many other cilia-dependent diseases, now termed ciliopathies. For a decade, mutations in the IFT genes and their relationship to ciliary sensory defects (chemo, mechano, and phtotosensory) received most of the research attention. A new aspect of IFT function has recently been discovered with data showing the role of IFT polypeptides in the process of exocytosis. IFT gene mutations, therefore, may not only affect ciliary assembly and function, but other cellular functions dependent on exocytosis. Among these are the roles of exocytosis and vesicle fusion with the cell membrane during cytokinesis promoting the formation of the cytokinetic furrow, and in vesicle exocytosis at the neuronal synapses and in formaiton of the immune synapse. Exocytosis and IFT are also important in the vesicle fusion at the base of the cilium which is required for ciliary membrane formation. Finally, another new role for eukaryotic cilia has recently been described, and that is the formation of exosomes or small vesicles from the ciliary membrane at the ciliary tip. It is felt that, in addition to being an organelle of motility and sensory function, the cilium may also be an important secretory organelle, signalling adjacent cells by means of these vesicles. #21 SYMPOSIUM - CILIA, SENSORY DYSFUNCTION AND DISEASE Genetic interactions dictate photoreceptor cilia biogenesis, homeostasis and survival Anand Swaroop National Eye Institute, Neurobiology Neurodegeneration & Repair Laboratory, Bethesda, Maryland Vertebrate photoreceptors are polarized post-mitotic neurons with a modified primary cilium that includes membrane discs and is critical for phototransduction. Photoreceptor cilium is a highly metabolically active organelle as almost 10% of outer segment discs are renewed everyday. Genetic defects that affect cilia biogenesis or transport process can lead to dysfunction or death of photoreceptors and consequently vision loss. We are specifically interested in two cilia-associated proteins CEP290 and RPGR and exploring their roles using zebrafish and mouse models. We find that these proteins interact with a specific set of NPHP and BBS proteins, and such interactions are critical for photoreceptor function and survival. #22 SYMPOSIUM - CILIA, SENSORY DYSFUNCTION AND DISEASE Loss of Bardet-Biedl Syndrome Proteins Causes Aberrant Localization of Ciliary GPCRs in Central Neurons Kirk Mykytyn The Ohio State University Columbus, OH, USA It has been known for more than forty years that neurons in the brain possess primary cilia, but the specific functions of these organelles remain unknown. Certain G protein-coupled receptors (GPCRs) specifically localize to neuronal cilia, suggesting they perform sensory and signaling functions on neurons. The functional importance of neuronal cilia is suggested by the fact that several human ciliopathies, including Bardet-Biedl syndrome (BBS), Joubert syndrome, and Meckel syndrome, have prominent functional and structural CNS phenotypes. BBS is characterized by obesity, retinal dystrophy, renal anomalies, hypogenitalism, polydactyly, and cognitive deficits. We have discovered that the BBS proteins are required for proper localization of GPCRs to primary cilia on neurons in the mouse brain. We hypothesize that some of the BBS phenotypes are the result of altered signaling due to ciliary GPCR mislocalization. Acknowledgements: National Institute of General Medical Sciences Abstracts are printed as submitted by the author(s) Abstracts | 13
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oom, without time keeping devices,
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#P113 POSTER SESSION III: OLFACTORY
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decreasing of endogenous volatiles
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may serve to integrate central and
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esponse magnitudes. Inhibitions rea
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the second a non-specific cation ch
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saline. Some of the labeled ORNs sh
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#P166 POSTER SESSION IV: CHEMOSENSO
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pregnancy block. In order to unders
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of GSP neurons and 97% of PA neuron
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concentrations than flies raised on
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familiarity and cultural difference
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#P265 is found on page 128. #P266 P
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perception of purine 5’-ribonucle
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#P278 POSTER SESSION VI: PERIPHERAL
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(CT), the greater superficial petro
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were significantly different from o
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MSG on NaCl is evidently highlighte
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consisting of motors and IFT comple
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wing. Philip Callahan exposed insec
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seem to indicate that total nasal v
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possibly suggesting non-apoptotic m
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#P325 POSTER SESSION VII: OLFACTORY
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of 7/10, and causing eyes to water
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showed that N1/P2 latencies were lo
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differentiated patients with AD (M=
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pleasantness 3)of mixtures (A,B), A
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Index Aarts, H - P328 Abe, K - P88,
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Haase, L - P3, P4, P29, P355 Haddad
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Murata, Y - P272 Murphy, C - P3, P4
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Veldhuizen, M - P7, P24, P25, P242,
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Registration 7:30 am to 1:00 pm, 6:
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See you next year! AChemS 33rd Annu
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Abstracts - Association for Chemoreception Sciences

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