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Circuit mechanisms underlying inhibitory gradients in piriform cortex
Anne-Marie M. Oswald, Adam M. Large and Nathan W. Vogler
Department of Neuroscience, Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA

The anterior piriform cortex (APC) is a trilaminar structure that processes odor information. Olfactory bulb afferents form layer 1a (L1a) and synapse with the apical dendrites of the principal excitatory neurons whose somas are found in L2/3. Principal neurons are also extensively recurrently connected through an intracortical fiber tract (L1b). Recent studies have shown that both afferent and intracortical excitatory connections are distributed randomly and uniformly over millimeter distances in APC [1,2]. In contrast, principal neurons receive asymmetric inhibition with stronger inhibition from caudal stimulation sites[3]. Using optogenetic activation of channelrhodopsin (ChR2) positive interneurons in slices from vGAT-ChR2 transgenic mice, we explore the spatial profile of inhibition for the three classes of principal excitatory neurons- L2 semilunar (SL) cells and superficial pyramidal cells (sPC) as well as deep L3 pyramidal cells (dPC). We find two gradients of inhibition. First, inhibition increases in strength from L1 to L3 stimulation sites as well from L2 to L3 principal cells, consistent with increasing interneuron counts from L1 to L3. This suggests potentially weaker feedforward inhibition via L1 interneurons and stronger recurrent inhibition through L2/3 interneurons. Second, inhibition onto L2 SL cells and sPCs is only weakly asymmetric whereas dPCs in L3 receive strong caudally biased inhibition. This suggests that within L2, inhibition and excitation may be approximately balanced. However, in L3 asymmetric inhibition may be unbalanced with respect to uniform recurrent excitation. We find that caudally biased inhibition onto dPCs is opposed by a rostrally-biased inhibition onto fast-spiking interneurons. We further investigated these inhibitory asymmetries in a transgenic mouse line that expresses ChR2 in somatostatin (Sst) interneurons. We find that asymmetric inhibition of dPCs may be mediated by a disinhibitory circuit whereby Sst interneurons inhibit fast-spiking interneurons that are presynaptic to the dPCs. Consistent with this model, the distribution of Sst(+) interneurons decreases along the rostral-caudal axis of APC. Taken together these results suggest two processing pathways one through L2 and the other L3. Each receives afferent and intracortical excitation but differ significantly in the strength and spatial profile of inhibition. The unique roles of these pathways in odor processing and the formation odor selective assemblies remain to be explored.

[1] Solsulski DL, et al. Nature 472:213-16 (2011).
[2] Franks KM, et al. Neuron 72:49-56 (2011).
[3] Luna VM, and Pettit Nature Neurosci. 13:533-35 (2010).