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2009 Abstracts - Association for Chemoreception Sciences

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neuron depletion. Adult mice were given 5-bromodeoxyuridine(BrdU) 3 weeks after unilateral bulbar injection of NMDA. Theywere killed 4 days, 2 wks, and 5 wks later. Similar to the effects ofbulbectomy, we found increased numbers of BrdU(+) cells at 4days in the epithelium on the treated side (112 vs 52 cells/mmcontralaterally). Surprisingly, there were also more BrdU (+)survivors on the treated side at 2 wks (32 vs. 24 cells/mm). By 5wks, numbers were similar to control counts, and survivingmature neurons persisted in the deprived epithelium as seen withdouble-labeling <strong>for</strong> olfactory marker protein. Within the<strong>for</strong>ebrain, bulb damage caused increased proliferation of SVZprogenitors, and these continued to migrate to the bulb in therostral migratory stream (RMS). By 2 wks, most BrdU (+) cells onthe normal side had reached the bulb, while on the lesioned side,most BrdU (+) cells were still contained within the RMS.Increased proliferation was accompanied by an increase in RMSvolume on the treated side (39.9 vs 19.1 mm 3 X 10-3 ), and an increasein TUNEL labeling. Labeling with neuronal markers showed thatnew neurons were added to the damaged bulb. These resultsindicate that some OSNs are capable of long-term survival afterdepletion of targets. Moreover, bulb injury significantly alters theproliferation and migration of SVZ/RMS precursors.#P221 Poster session V: Chemosensory memory/Central synaptic physiology/NeurogenesisGlomerular Regulation of Mitral Cell Responses toSensory InputZuoyi Shao, Adam C. Puche, Michael T. ShipleyDepartment of Anatomy & Neurobiology, Program inNeuroscience, University of Maryland School of MedicineBaltimore, MD, USAOlfactory signals are initially processed in glomeruli, whereolfactory nerve (ON) axons <strong>for</strong>m excitatory synapses ontoprincipal output neurons, mitral/tufted (M/T) cells. M/T cells arethought to be regulated mainly by inhibition at their lateraldendrites from GABAergic granule cells (GC) but less is knownabout inhibition occurring at their glomerular tuft fromGABAergic periglomerular (PG) cells. We examined the relativecontributions of glomerular and infraglomerular inhibition ofmitral cells in bulb slices. ON stimulation produces an initialmonosynaptic EPSC in mitral cells that is interrupted by a shortlatency burst of IPSCs followed by a protracted train ofintermittent IPSCs. Addition of APV, which has been shown toblock the M/T-GC feedback circuit, significantly reduced lateIPSCs suggesting that they derive from GCs, but had little effecton the early IPSC barrage. In contrast, microinjection of gabazine(GBZ) into glomeruli blocked the early burst of IPSCs but hadlittle effect on the late IPSCs. How does this affect mitral celloutput? Mitral cells respond to ON input with a long lastingdepolarization (LLD) upon which rides an initial short latencyspike burst followed by sparse later spikes. Removal of M/T-GCinhibition with APV had little effect on M/T spike responses toON stimulation. However, microinjection of GBZ to blockglomerular inhibition increased M/T spike output ~30-fold.Glomerular inhibition also dramatically regulated the magnitudeand duration of mitral cell LLDs. These data suggest glomerularinhibition is a much more potent regulator of mitral cell responsesto sensory input that previously considered.#P222 Poster session V: Chemosensory memory/Central synaptic physiology/NeurogenesisCharacteristics of spontaneous and evoked EPSCs ofinterneurons in the superficial external plexi<strong>for</strong>m layerof olfactory bulbYu-Feng Wang, Kathryn A HamiltonLSU Health <strong>Sciences</strong> Center- Shreveport Shreveport, LA, USAInterneurons in several olfactory bulb layers are excited bymitral/tufted cells and provide feedback/lateral inhibition thatshapes M/T cell spontaneous spiking/bursting and responses toolfactory input. At some M/T cell-interneuron synapses, AMPAreceptors mediate fast interneuron excitation that results in fastM/T cell inhibition. At other synapses, NMDA receptors mediateslower interneuron excitation that results in slower, prolongedM/T cell inhibition. Here, we characterized spontaneous EPSCsof interneurons in the superficial EPL of mouse olfactory bulbslices and responses of cells in this region to glomerular-layerstimulation. Most superficial interneurons (26/27) spontaneouslygenerated EPSC clusters. EPSC frequency within clusters (112.2 ±9.4.0 Hz) was significantly higher than be<strong>for</strong>e clusters (37.5 ± 3.8Hz, P

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