Parvalbumin (PV)-expressing interneurons mediate fast inhibition of principal neurons in many brain areas; however, long-term plasticity at PV-interneuron output synapses has been less well studied. In the auditory cortex, thalamic inputs drive reliably timed action potentials (APs) in principal neurons and PV-interneurons. Using paired recordings in the input layer of the mouse auditory cortex, we found a marked spike-timing-dependent plasticity (STDP) at PV-interneuron output synapses. Long-term potentiation of inhibition (iLTP) is observed upon postsynaptic (principal neuron) then presynaptic (PV-interneuron) AP firing. The opposite AP order causes GABAB-mediated long-term depression of inhibition (iLTD), which is developmentally converted to iLTP in an experience-dependent manner. Genetic deletion of GABAB receptors in principal neurons suppressed iLTD and produced deficits in auditory map remodeling. Output synapses of PV-interneurons thus show marked STDP, and one limb of this plasticity, GABAB-dependent iLTD, is a candidate mechanism for disinhibition during auditory critical period plasticity.
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