| First Author | Vickers ED | Year | 2018 |
| Journal | Neuron | Volume | 99 |
| Issue | 4 | Pages | 720-735.e6 |
| PubMed ID | 30078579 | Mgi Jnum | J:267945 |
| Mgi Id | MGI:6269057 | Doi | 10.1016/j.neuron.2018.07.018 |
| Citation | Vickers ED, et al. (2018) Parvalbumin-Interneuron Output Synapses Show Spike-Timing-Dependent Plasticity that Contributes to Auditory Map Remodeling. Neuron 99(4):720-735.e6 |
| abstractText | 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. |
