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Published on: January 18, 2013
Differences in Glomerular-Layer-Mediated Feedforward Inhibition onto Mitral and Tufted Cells Lead to Distinct Modes
Matthew Geramita1, Nathan N Urban2
1Department of Neurobiology, Center for Neuroscience at the University of Pittsburgh, Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, Pennsylvania 15213.
Abstract:
Understanding how each of the many interneuron subtypes affects brain network activity is critical. In the mouse olfactory system, mitral cells (MCs) and tufted cells (TCs) comprise parallel pathways of olfactory bulb output that are thought to play distinct functional roles in odor coding. Here, in acute mouse olfactory bulb slices, we test how the two major classes of olfactory bulb interneurons differentially contribute to differences in MC versus TC response properties. We show that, whereas TCs respond to olfactory sensory neuron (OSN) stimulation with short latencies regardless of stimulation intensity, MC latencies correlate negatively with stimulation intensity. These differences between MCs and TCs are caused in part by weaker excitatory and stronger inhibitory currents onto MCs than onto TCs. These differences in inhibition between MCs and TCs are most pronounced during the first 150 ms after stimulation and are mediated by glomerular layer circuits. Therefore, blocking inhibition originating in the glomerular layer, but not granule-cell-mediated inhibition, reduces MC spike latency at weak stimulation intensities and distinct temporal patterns of odor-evoked responses in MCs and TCs emerge in part due to differences in glomerular-layer-mediated inhibition.SIGNIFICANCE STATEMENT Olfactory bulb mitral and tufted cells display different odor-evoked responses and are thought to form parallel channels of olfactory bulb output. Therefore, determining the circuit-level causes that drive these differences is vital. Here, we find that longer-latency responses in mitral cells, compared with tufted cells, are due to weaker excitation and stronger glomerular-layer-mediated inhibition.
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