Abstracts - Association for Chemoreception Sciences

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P O S T E R S #P213 POSTER SESSION V: CENTRAL OLFACTION; CHEMOSENSORY PSYCHOPHYSICS & CLINICAL STUDIES An Ih-dependent Switch from Inhibition to Excitation in ET Cells by Co-release of GABA and DA from SA Cells Zuoyi Shao, Shaolin Liu, Adam C. Puche, Michael T. Shipley Department of Anatomy & Neurobiology, Program in Neuroscience, University of Maryland School of Medicine Baltimore, MD, USA Olfactory bulb short axon (SA) cells co-express DA and GABA and form multiglomerular circuits spanning 10’s-100s of glomeruli. ET cells receive direct ON input and provide excitatory drive to SA, PG and mitral/tufted (MT) cells. Thus modulation of ET cells significantly impacts glomerular processing and OB output to olfactory cortex. There is evidence that ET cells receive synaptic input from the GABA-DAergic SA cells. How does co-release of DA and GABA influence ET cells? ET cells respond to stimulation of SA cell interglomerular circuit with short latency hyperpolarization followed by a strong rebound depolarization that generates a burst of action potentials. Both the initial hyperpolarization and the rebound spike burst were blocked by gabazine. Brief hyperpolarization of ET cells leads to strong rebound depolarization due to activation of a prominent Ih current. Thus, ET cell hyperpolarization mediated by SA cell GABA release might activate Ih triggering the rebound spike burst. In many CNS neurons DA enhances Ih. Indeed, bath applied DA (in the presence of fast synaptic blockers) increased Ih in ET cells. Thus co-release of DA by SA cells might strengthen the GABA-induced rebound excitation. Consistent with this hypothesis, upon SA stimulation the rebound depolarization, but not the initial hyperpolarization, was significantly attenuated by D1-like antagonists. ET cells drive PG cells, which inhibit MT cells. Thus the net result of SA cell activation may be to generate interglomerular inhibition of MT cells. Further, the present findings demonstrate a novel neural mechanism whereby synaptic inhibition is transformed into strong excitation by target cell intrinsic properties and DA modulation. Acknowledgements: Supported by NIH NIDCD DC005676 #P214 POSTER SESSION V: CENTRAL OLFACTION; CHEMOSENSORY PSYCHOPHYSICS & CLINICAL STUDIES Olfactory-visual integration facilitates perceptual discrimination of facial expressions Emily Cahill, Lucas Novak, Wen Li University of Wisconsin-Madison Madison, WI, USA Multisensory integration markedly improves perception of a stimulus, especially when the sensory input is minimal (known as “the rule of inverse effectiveness”). Research has largely focused on cross-modal interactions among senses other than olfaction, implicating the thalamus as a primary neural substrate in this process. Given that olfactory input bypasses this structure en route to the primary olfactory cortex, this theory is unlikely to figure well in olfaction-related sensory merging. It thus remains to be explored how olfactory information interacts with other sensory stimulation. In this study, we examined the effect of odor on the discrimination of two highly similar faces using a dotprobe paradigm in combination with brain event-related potentials. On a given trial, we delivered an unpleasant or neutral odor for 2 sec, and then presented a pair of faces simultaneously in the left and right visual fields for 400ms, followed by a dot appearing at the location of either of the faces. In each pair, one face contained a neutral expression and the other face the neutral expression morphed with 12.5% of fearful expression of the same person. Despite that a two-alternative-forced-choice task confirmed that these faces were indistinguishable, a visual ERP component, P1, appearing at 90 ms post-stimulus indicated visual discrimination of the faces in the presence of unpleasant (vs. neutral) odors, varying as a function of the level of anxiety of the subjects (P
#P216 POSTER SESSION V: CENTRAL OLFACTION; CHEMOSENSORY PSYCHOPHYSICS & CLINICAL STUDIES Glutamate modulates inhibitory inputs of GABAergic interneurons in the superficial EPL of the main olfactory bulb Yu-Feng Wang, Kathryn A Hamilton LSUHSC Shreveport, LA, USA The superficial external plexiform layer (sEPL) of the main olfactory bulb (OB) contains GABAergic interneurons (INs), many of which exhibit spontaneous EPSCs mediated by AMPA receptors and modulated by presynaptic NMDA receptors. Here, we show that AMPA and NMDA receptor-mediated excitation also modulates IN inhibition. In OB slices from transgenic mice expressing eGFP under control of the promoter for the GAD65 gene, many eGFP + sEPL INs exhibited spontaneous IPSCs (sIPSCs) that were blocked by the GABAA receptor antagonists gabazine (GZ) or bicuculline. In the presence of TTX, glutamatergic modulation of miniature IPSCs (mIPSCs) was observed. The NMDA receptor antagonist APV reduced the mIPSC duration, but it did not affect mIPSC amplitude and frequency. The AMPA receptor antagonist CNQX had similar effects, and it also accelerated the mIPSC rising slope. In the presence of APV and CNQX, high K + stimulation could still evoke mIPSCs, suggesting that presynaptic glutamate receptors modulate GABA release. Stimulation of the EPL evoked shortlatency IPSCs (eIPSCs), which were blocked by GZ and TTX. Both APV and CNQX reduced the latency of the eIPSCs. Dual-pulse stimulation resulted in depression (PPD) of the paired eIPSC; PPD was not affected by APV or CNQX, but CNQX changed the ratio of rising slope of the paired eIPSC. In Mg 2+ free ACSF, PPD and effects of APV and CNQX on paired eIPSCs were not observed. These results indicate that glutamatergic synapses modulates GABAergic inhibition of sEPL INs. Acknowledgements: NIH DC007876 #P217 POSTER SESSION V: CENTRAL OLFACTION; CHEMOSENSORY PSYCHOPHYSICS & CLINICAL STUDIES Ion Channel in the Olfactory Bulb Subserves as a Metabolic Sensor Kristal R. Tucker 1 , Melissa Cavallin 1 , J. Michael Overton 2 , Debra A. Fadool 1,3 1 Program in Neuroscience, Department of Biological Science, Florida State University Tallahassee, FL, USA, 2 College of Medicine, Department of Biomedical Sciences, Florida State University Tallahassee, FL, USA, 3 Programs in Neuroscience and Molecular Biophysics, The Florida State University Tallahassee, FL, USA Naturally occurring modulators of the Kv1.3 ion channel, as expressed in mitral cells, include the insulin receptor and the TrkB neurotrophin receptor - both of which have been implicated in other parts of the CNS to modulate metabolism. We now demonstrate via slice electrophysiology that mitral cell action potential firing properties are sensitive to another metabolically important substance, glucose. Like the hypothalamus, we have found the olfactory bulb contains two populations of glucosesensitive mitral cells; glucose excited and glucose inhibited. Gene-targeted deletion or acute suppression of Kv1.3 results in an overall increased mitral cell sensitivity via increased-current evoked spiking frequency, decreased latency to first spike, and a more depolarized resting membrane potential. To explore the correlation between Kv1.3, metabolism, and olfaction, 11 week old mice were maintained on a moderately high fat diet (MHF, 32% fat) for 26 weeks and then systems physiological parameters of body weight, respiration, locomotion, and ingestive behaviors were quantified in a custom designed, computer interfaced, metabolic chamber. Diet-induced obese (DIO) mice exhibited a 47% increase in body weight, a 32% increase in serum insulin, and a loss of 52% of M72-expressing olfactory sensory neurons (OSNs). Kv1.3-null mice were resistant to DIO with a weight gain of only 10% and no change in adiposity as a result of a significant increase in basal metabolic rate linked to the MHF challenge. Bilateral olfactory bulbectomy (OBX) in a Kv1.3-null background yielded mice that were no longer resistant to DIO. The mice exhibited a 30% increase in body weight via preventing the increase in basal metabolic rate in response to the MHF challenge, which resulted in a decreased activity-dependent metabolism. Acknowledgements: NIH NIDCD R01DC003387 & F31DC010097 and the TMH/Robinson Foundation. #P218 POSTER SESSION V: CENTRAL OLFACTION; CHEMOSENSORY PSYCHOPHYSICS & CLINICAL STUDIES The Expression Pattern of TrpM5 and NT-3 in the Ventral Main Olfactory Bulb of Mice Reveals Two Distinct Populations of Glomeruli Shane H Rolen, Thomas E Finger, Diego Restrepo Rocky Mountain Taste & Smell Center & Dept. Cell & Developmental Biology, Univ Colorado Denver School of Medicine Aurora, CO, USA Previous investigations in mice demonstrated that the transient receptor potential channel M5 (TrpM5) and neurotrophin-3 (NT- 3) are expressed by a subset of olfactory sensory neurons (OSNs) located in the main olfactory epithelium. OSNs expressing high levels of either TrpM5 or NT-3 project to glomeruli located in the ventral regions of the main olfactory bulb (vMOB). The TrpM5 + glomeruli of this region process semiochemical information including odors of urine. The goal of the current study is to determine whether the OSNs expressing TrpM5 or NT-3 project the same or discrete populations of glomeruli in the vMOB. We bred TrpM5-GFP/NT-3-LacZ mice where GFP is expressed under the control of TrpM5 promoter and the coding region for NT-3 was replaced by E. coli lacZ thus the expression of b- galactosidase mimics the expression of NT-3. Standard fluorescent immunocytochemical protocols were utilized to label and visualize both GFP and b-galactosidase. The expression pattern of GFP and b-galactosidase observed in the current investigation was consistent with results reported in previous investigations, i.e. glomeruli in the vMOB are strongly positive for one or the other of the markers. In the current study, preliminary analysis suggests that glomeruli that are strongly labeled for GFP or b-galactosidase constitute two largely separate populations. The results of the current investigation suggests that strongly labeled NT-3 + glomeruli in the vMOB represent a distinct subset, separate from the TrpM5 + population. Future studies are needed to determine if NT-3 + glomeruli participate in processing urine or semiochemical odor information. Acknowledgements: Supported by grants from the NIH and BNAT. P O S T E R S Abstracts are printed as submitted by the author(s) Abstracts | 99
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AChemS Association for Chemorecepti
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AChemS Association for Chemorecepti
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We are pleased to announce that sev
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#1 GIVAUDAN LECTURE Normal and Canc
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and against delta ENaC is being pur
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#13 SYMPOSIUM - GENETICS OF HUMAN O
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#19 SYMPOSIUM - CILIA, SENSORY DYSF
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#26 PLATFORM PRESENTATIONS - POLAK
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esponse selectivity for both OSNs a
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elicit glucagon-like peptide-1 (GLP
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contrast, changing the concentratio
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of OBPs, we have systematically sup
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whereas mouse and joystick reaction
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POSTER PRESENTATIONS #P1 POSTER SES
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PROP strips and PROP solutions. PAV
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#P11 POSTER SESSION I: TASTE IMAGIN
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TGI. The present study investigated
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delivered in the scanner intra-oral
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a universal odor descriptor map. Ho
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acetate or ethyl butyrate v/v in mi
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#P54 POSTER SESSION II: OLFACTORY P
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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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