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Abstract
The anterior piriform cortex (APC) is thought to be a site of odor encoding. The proximity to odor sensory input makes the APC highly tractable for dissecting the role of cortical circuitry in sensory processing. However, the trilaminar circuit structure of the APC is similar to that of the hippocampus, suggesting a potentially associative role in learned odor representations. Indeed, associative long-term potentiation (LTP) can be elicited using a standard theta burst stimulation (TBS) paradigm. However, it is not known if there is commensurate plasticity at inhibitory synapses within APC.
We investigated excitatory and inhibitory synaptic plasticity in APC following criterion performance in an olfactory discrimination task. We used targeted recombination in active populations (TRAP) to conditionally express tdTomato in pyramidal neurons (PNs) that were active during the task. We found that in trained animals, recurrent excitation and inhibition are potentiated in tdTom+ neurons compared to tdTom- neurons. To investigate the synaptic locus of inhibitory plasticity, we bred triple transgenic mice that allow TRAP expression in PNs along with cre-dependent ChR2 expression in parvalbumin (PV) or somatostatin (SST) interneurons (IN). Following learning, we then recorded light evoked inhibitory currents onto tdTom+ and tdTom-neurons in APC. We found that PV mediated inhibition tended to be stronger onto tdTom+ PNs compared to tdTom- PNs while SST-mediated inhibition trended weaker or unchanged.
Finally, we investigated whether PV or SST mediated inhibitory plasticity could be elicited through an associative LTP mechanism. To selectively recruit PV or SST inhibition we expressed ChR2 in PV or SST INs and evoked IPSCs pre and post aLTP induction. To preserve SST or PV mediated inhibition and to drive the necessary VIP-disinhibitory circuit, we thus applied cholinergic agonists during induction and assessed changes in EPSC and IPSC amplitudes 30 min following induction compared to baseline. We found that the muscarinic agonist, carbachol, unreliably promoted LTP of EPSCs, contrary to previous reports. We also found that the nicotinic agonist, epibatidine, promoted inhibitory LTD in the SST cell population. Together this work demonstrates inhibitory plasticity of both PV and SST cell types and a putative mechanism by which plasticity occurs.