Abstracts - Association for Chemoreception Sciences

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This interplay could be mediated by neuroendocrine signals like insulin and/or leptin as their receptors have been described at peripheral (olfactory epithelium) and central (olfactory bulb, OB) levels. To test this hypothesis, we studied the modulation of the activity of the olfactory sensory neurons (OSN) by hormonal peptides. Using patch-clamp recordings in an in vitro intact epithelium, we showed that insulin- or leptin-perfusion significantly raises the spontaneous firing frequency of the OSN. Moreover, these hormones decrease the OSN transduction current and receptor potential recorded during odorant stimulation. Therefore by increasing the spontaneous activity but reducing the odorant-induced activity of OSN, an elevated insulin and leptin level may result in a decreased global signal to-noise ratio in the olfactory epithelium. This input to the bulb is further modulated by the main output neurons of the OB (mitral cells, MC). The MC are one of the central targets of these hormones: MC express insulin receptors and their discharge is modulated by insulin or leptin. This effect would underlie our behavioral tests where an icv injection of either insulin or leptin decreases olfactory detection. Thus insulin and leptin act in the olfactory system both at peripheral and OB levels to modulate olfactory sensitivity. The role of olfaction in the control of food intake appears crucial and needs to be investigated further in order to better understand alimentary pathologies. Acknowledgements: This grant was supported by the Agence Nationale de la Recherche (ANR), the French national research agency (project ANR-05-PNRA-1.E7 AROMALIM) #37 SYMPOSIUM - CHEMORECEPTION IN CONTEXT: INTERACTIONS WITH ENDOCRINE SYSTEMS AND METABOLIC STATE The olfactory bulb as a metabolic sensor via insulin modulation Debra A. Fadool 1,2 , Kristal Tucker 2 , David R. Marks 2 , Melissa A. Cavallin 2 , James M. Overton 3 , Paola Pedarzani 4 1 Florida State University Program in Neuroscience and Molecular Biophysics Tallahassee, FL, USA, 2 Florida State University Department of Biological Sciences Tallahassee, FL, USA, 3 Florida State University Department of Biomedical Sciences and Program in Neuroscience Tallahassee, FL, USA, 4 Research Department of Neuroscience, Physiology and Pharmacology, University College London London, United Kingdom Gene-targeted deletion of a predominant voltage-dependent potassium channel, Kv1.3, in mitral cells of the olfactory bulb results in a gamut of phenotypic changes including a “supersmeller” ability, supernumerary axonal projections to heterogenous glomeruli, and an alternation in action potential discharge frequency. Kv1.3 is a substrate for tyrosine phosphorylation and the molecular targets for modulation by the hormone insulin have been mapped along the N- and C-termini of the channel. Our laboratory has developed awake, intranasal insulin delivery approaches that demonstrate a robust phosphorylation of the channel that is linked to the behavioral but not anatomical modifications of the knockout model. Recently the laboratory has discovered that the channel is also responsible for regulating body weight and that both diet- and geneticallyinduced obesity can be abrogated via gene-targeted deletion of the channel, or uniquely by olfactory bulbectomy that manipulates total energy expenditure. We have now recorded on acute and chronic insulin treated mice as well as diet-induced obese mice and will present an electrophysiological analysis performed on brain slices of how metabolic state alters neuronal responses in mitral cells of the olfactory bulb. High fat diet has additionally demonstrated an anatomical loss of olfactory sensory neurons, presynaptic to the mitral cell input. Acknowledgements: This work was supported by NIH DC03387 and NIH DC00044 from the NIDCD and sabbatical award from FSU. #38 SYMPOSIUM - CHEMORECEPTION IN CONTEXT: INTERACTIONS WITH ENDOCRINE SYSTEMS AND METABOLIC STATE Roles of taste signaling molecules in endocrine cells in pancreas and tongue Zaza Kokrashvili, Peihua Jiang, Bedrich Mosinger, Robert F. Margolskee Monell Chemical Senses Center Philadelphia, PA, USA Ga-gustducin, T1r receptors and other taste signaling elements are expressed in duodenal enteroendocrine L cells that express insulinotropic glucagon-like peptide 1 (GLP-1). Gustducin and T1r3, well known for their roles in taste signaling, are essential for L cell release of GLP-1 in response to glucose. We examined taste cells to determine if they too expressed hormones typical of intestinal enteroendocrine cells. Taste cells were found to express GLP-1, glucagon, PYY and other gut hormones. Patterns of expression indicated that gustducin-expressing type II taste cells and other subtypes of taste cells express GLP-1. We also examined the function of hormones released from these “endocrine taste cells”. In wild-type mice, with or without esophagealectomy/ vagotomy, application of glucose to the tongue induced a rapid elevation of GLP-1 in the bloodstream. Stimulation of taste cell explants from wild-type mice with glucose led to release of GLP-1 into the medium. Stimulation of gustducin-null mice with glucose did not lead to significant release of GLP-1 from taste cells in vivo or in explants. At least a portion of the cephalic phase rise in circulating GLP-1 depends on direct release of GLP-1 from taste cells into the bloodstream and requires gustducin. Taste receptors, Ga-gustducin and downstream proteins were also found to be expressed in several types of pancreatic islet cells. Ga-gustducin is expressed in alpha cells, and T1R3 is expressed in alpha and beta cells. Functional assays showed that in wild type mice, but not in T1R3 null mice, T1R3 receptors mediate increased secretion of insulin in response to artificial sweeteners and sweet tasting amino-acids. Acknowledgements: Supported by NIH grants DC03055 and DC03155 to RFM #39 SYMPOSIUM - CHEMORECEPTION IN CONTEXT: INTERACTIONS WITH ENDOCRINE SYSTEMS AND METABOLIC STATE Mechanisms of alimentary chemosensation and modulation C. Shawn Dotson 1 , Amanda E.T. Elson 2 , Steven D. Munger 2 1 Department of Neuroscience & Center for Smell and Taste, University of Florida College of Medicine Gainesville, FL, USA, 2 Department of Anatomy & Neurobiology, University of Maryland School of Medicine Baltimore, MD, USA Chemosensory cells throughout the alimentary canal use a common molecular toolkit to detect and respond to nutrients and other chemostimuli. For example, “taste” transduction molecules (e.g., TAS1R and TAS2R receptors, gustducin) regulate hormonal secretion in the gut. We have reported that a loss-of-function variant of a human TAS2R is associated with glucose dysregulation and the presence of Type 2 diabetes mellitus in a human population. Furthermore, bitter-tasting compounds can 18 | AChemS Abstracts 2010 Abstracts are printed as submitted by the author(s)
elicit glucagon-like peptide-1 (GLP-1) secretion from enteroendocrine L cells in a receptor-dependent manner, thus suggesting a mechanism by which TAS2R function could influence glucose homeostasis. Interestingly, “gut” hormones (e.g., GLP-1) can modulate peripheral taste function as well. We found that both GLP-1 and glucagon modulate sweet taste sensitivity. GLP-1 is produced in two distinct subsets of mammalian taste cells, while the GLP-1 receptor is expressed on adjacent intragemmal afferent nerve fibers. In contrast, glucagon and its receptor are coexpressed in a distinct population of taste cells. However, both GLP-1 and glucagon signaling appear to enhance or maintain sweet taste sensitivity: genetic and/or pharmacological disruption GLP-1 or glucagon signaling results in dramatically reduced taste responses to sweeteners in behavioral assays. Together, our recent studies of the interplay between gustatory and endocrine systems support a role for canonical “taste” molecules in the maintenance of metabolic homeostasis and suggest that sensory function may be modulated in the context of an animal’s metabolic status. Acknowledgements: Supported by: NIDCD (R01 DC005786, R01 DC010110, F31 DC010113, T32 DC000054, P30 DC010364), NIDDK (P30 DK072488), NIDCR (T32 DE007309) and the Ajinomoto Amino Acid Research Program. #40 SYMPOSIUM - WIRING THE OLFACTORY SYSTEMS Mapping Odorant Receptor Classes in the Mouse Olfactory Bulb Thomas Bozza, Rodrigo Pacifico, Jingji Zhang, and Brian Weiland Department of Neurobiology and Physiology, Northwestern University,Evanston, IL, United States Olfactory sensory neurons that express defined odorant receptors form specific glomeruli at relatively reproducible positions in the mouse olfactory bulb. The spatial arrangement of glomeruli likely plays a role in odor processing. It has been known for decades that odorants with certain functional groups can preferentially activate glomerular domains in the rodent olfactory bulb. However, the molecular underpinnings of this functional organization remain unclear. We have shown that sensory neurons expressing phylogenetically-distinct classes of odorant receptors map to discrete domains in the olfactory bulb. Despite the fact that odorant receptors influences axon guidance, the classspecific projections are independent of the expressed odorant receptor. Our hypothesis is that the domains are formed by axons from different lineages, or types, of olfactory sensory neurons, each with a distinct axon guidance identity. These sensory neuron types contribute to the functional organization of the glomerular array. This hypothesis has implications for mechanisms of odor mapping in the mammalian olfactory bulb. #41 SYMPOSIUM - WIRING THE OLFACTORY SYSTEMS Axon - matrix interactions regulate olfactory wiring Helen B. Treloar 1 , Arundhati Ray 1 , Lu Anne V. Dinglasan 1 , Melitta Schachner 3,4 , Charles A. Greer 1,2 1 Department of Neurosurgery, Yale University School of Medicine New Haven, CT, USA, 2 Department of Neurobiology, Yale University School of Medicine New Haven, CT, USA, 3 Zentrum für Molekulare Neurobiologie, Universitätskrankenhaus Hamburg-Eppendorf Hamburg, Germany, 4 Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University Piscataway, NJ, USA Olfactory sensory neuron (OSN) axons follow stereotypic spatiotemporal paths in the establishment of the olfactory pathway. The topography of olfactory projections from epithelium to olfactory bulb (OB) is an essential determinant of odor coding. The mechanisms subserving the sorting and targeting of axons are complex. Recent studies highlight the importance of guidance molecules including odor receptor proteins which have been shown to be necessary for correct targeting. We have identified extracellular matrix (ECM) molecules expressed early in the developing pathway which we have proposed to play a role in its initial establishment. During later embryonic development, when axons sort out and target specific glomeruli, we have hypothesized that ECM cues may also act to help establish the complex olfactory topography. In a screen of ECM molecules expression during the period of glomerulogenesis we identified tenascin-C (TNC) in a boundary-like expression pattern, which appears to prevent axons from prematurely innervating deeper layers of the OB and initiating glomerulogenesis. To investigate this hypothesis we developed an in vitro assay of OSN neurite outgrowth and demonstrate that TNC is inhibitory in a dose dependent manner, and axons avoid growing on TNC substrates in stripe assays. Analysis of glomerulogenesis in TNC null mice reveals that glomerular development is delayed in the absence of TNC. These data correlate with previously published behavioral reports of TNC null mice which display impaired olfactory function in the early postnatal period, but recover function over the first postnatal week (de Chevigny et al. 2006 Mol Cell Neurosci. 32:174-86). Together, these data demonstrate that TNC acts to restrict OSN axons to the nerve layer during a key period of olfactory pathway development. Acknowledgements: Supported by NIH DC005706 and DC007600 to HBT, HHMI and NIH-NHLBI Fellowships to LVD, Deutsche Forschungsgemeinschaft to MS, and NIH DC00210 to CAG. #42 SYMPOSIUM - WIRING THE OLFACTORY SYSTEMS Faf1 as a Regulator of Olfactory Axon Guidance Leonardo Belluscio, Kai Cheng National Institutes of Health / NINDS Bethesda, MD, USA The mammalian olfactory system provides an excellent in-vivo model to study axon guidance through its precise connections which link the peripheral olfactory epithelium to the centrally located olfactory bulb (OB). Since axons of olfactory sensory neurons (OSNs) project to specific targets in the OB, the system offers a predictable pattern from which to evaluate changes in axon guidance. As apoptosis signaling has been implicated in the process of axon guidance we used the olfactory system to explore this connection by focusing on the apoptotic signaling molecule, Fas-Associated Factor 1 (Faf1). Faf1 has been shown to play a Abstracts are printed as submitted by the author(s) Abstracts | 19
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familiarity and cultural difference
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perception of purine 5’-ribonucle
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(CT), the greater superficial petro
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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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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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