2009 Abstracts - Association for Chemoreception Sciences

ain region was isolated. Then, Cy3 labeled cRNA washybridized to whole rat genome chips. Out of 28,142 genespresent in each brain region, 251 (PBN), 113 (CeA/BLA), and103 (LH) showed up or down regulation of at least 2 fold and ap value ≤ 0.05. When considering only p values ≤ 0.001, thenumber of differentially expressed genes in PBN, amygdala, andLH decreased to 37, 27, and 22, respectively. Relative to controlanimals, CTA acquisition altered the expression of variouspeptides, transcription factors, phosphatases, kinases, receptorsand ion channels. Directional change in expression of subsets ofgenes was confirmed using quantitative real-time RT-PCR. Thepresent data provide a starting point for understanding geneexpression specific to gustatory and aversive visceral stimulation,as well as learning dependent modulation of gustatory palatability.#P214 Poster session V: Chemosensory memory/Central synaptic physiology/NeurogenesisExpression of Transient Receptor Potential (TRP) Channelsin the Mouse Main Olfactory Bulb (MOB)Hong-Wei Dong 1 , Sheng-Yuan Ding 2 , Qiang Nai 1 ,Fu-Ming Zhou 2 , Matthew Ennis 11Dept, Anat &Neurobiology, University of Tennessee, HSCMemphis, TN, USA, 2 Dept. Pharmacology, University ofTennessee, HSC Memphis, TN, USATRP channels are a large family of cation channels with widedistribution in the CNS. TRP channels are involved in sensoryprocessing in the visual, gustatory, olfactory, auditory andsomatosensory pathways. Currently, 28 TRP gene subtypes havebeen identified and subdivided into 6 families (TRPC1-7, TRPV1-6, TRPM1-8, TRPP2-3, 5, TRPML1-3 and TRPA2). The MOBhas been reported to express several TRP channel subtypes.However, the full expression profile of the TRP channel family inthe MOB has not been investigated, and very little is known aboutTRP channel expression in different MOB cell types. In presentstudy, we employed MOB tissue and single-cell RT-PCR methodsto investigate the expression of 28 TRP channel mRNAs in themouse MOB. Our results showed that TRPC1-7, TRPV2, 4,TRPM2-4, 6-8, TRPP2-3, 5 TRPML1-2 and TRPA2 mRNA wereexpressed in the MOB. To date, TRPC4-5 were detected inelectrophysiologically identified external cells and periglomerularcells whereas TRPC3, TRPC5, TRPV4 and TRPM2-3, 7-8 weredetected in electrophysiologically identified mitral cells.#P215 Poster session V: Chemosensory memory/Central synaptic physiology/NeurogenesisCholinergic modulation of glomerular circuitsShaolin Liu, Michael T. ShipleyUniversity of Maryland School of Medicine Baltimore, MD, USAThe olfactory bulb receives cholinergic (ACh) afferents from thebasal forebrain. These inputs are activated in a behavioral statedependentmanner. There are open questions about the impact ofACh inputs, particularly at the level of glomerular circuits. ONsynapses activate external tufted (ET) cells, which strongly exciteGABAergic periglomerular (PG) cells. PG cells providepresynaptic inhibition of ON terminals, postsynaptic inhibitionto MT cells as well as feedback inhibition to ET cells. Thusintraglomerular circuits generate inhibition at several points toshape the transfer of sensory signals to output neurons.With GABA A and GABA B Rs blocked, either nicotine (N)or a muscarinic (M) receptor agonist, milameline, significantlyreduced spontaneous EPSCs in PG but not ET cells, indicatingthat ACh suppresses ET cell excitation of PG cells via both Nand M ACh receptors. With fast glutamate Rs blocked,carbamylcholine, which activates both N and M receptors,significantly enhanced spontaneous IPSCs in both ET and PGcells. Scopolamine blocked and milameline replicated these effectsindicating that activation of M receptors increases intraglomerularrelease of GABA. ACh appears to reduce ET cell excitatory driveon PG cells, yet increases PG cell release of GABA. We areinvestigating whether ACh increases PG cell GABA release byaction potential-dependent/-independent mechanisms. Increasedintraglomerular GABA release may presynaptically inhibit ONinputs via GABA B receptors and postsynaptically inhibit MToutput firing via GABA A receptors. Behavioral state-dependentactivation of cholinergic inputs might contribute to increasedcontrast among glomeruli differentially activated by sensorysignals.#P216 Poster session V: Chemosensory memory/Central synaptic physiology/NeurogenesisSynchronization of spike activity in tufted cells of mouseolfactory bulbGraeme Lowe, Jie MaMonell Chemical Senses Center Philadelphia, PA, USASynchronization of principal cell spiking in the olfactory bulb isproposed to play a role in odor coding. Synchrony occurs inmitral cells linked to the same glomerulus, but has not beenanalyzed in tufted cells. We recorded spontaneous spiking frommitral and tufted cell pairs in mouse olfactory bulb slices andperformed cross correlation analyses on spike trains. Synchronousbursting and spiking were manifested as broad and narrow peaksin spike cross-correlograms from mitral-mitral, mitral-tufted andtufted-tufted pairs linked to the same glomerulus, but not todifferent glomeruli. Slow EPSCs were synchronized in mitraltuftedand tufted-tufted pairs linked to the same glomerulus.Spike synchrony was uncorrelated with burst synchrony,suggesting independent synchronization mechanisms. On average,spike synchrony was stronger and spike lags shorter in tuftedtufted,than in mitral-tufted or mitral-mitral pairs. All paircombinations exhibited electrical coupling, with largest meancoupling coefficient in tufted-tufted pairs. Spike synchrony wasnot fully blocked by the AMPA receptor antagonist NBQX forany pair combination, and was abolished by NBQX plus NMDAreceptor antagonist dichlorokynurenic acid only in mitral-mitralpairs. Our results suggest that glomerulus-specific spikesynchrony in olfactory bulb principal cells depends primarily ongap junctions, and may be enhanced by mutual excitation viaionotropic glutamate receptors. Glomeruli may split sensoryinformation into parallel data streams conveyed by mitral andtufted cells, encoding different aspects of odor stimuli. Spikesynchronization provides a substrate for temporal binding ofolfactory receptor identity for these parallel streams, even if theyare received and decoded by distinct cortical circuits.94 | AChemS Abstracts 2009