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Neuron. 2019 Jan 2;101(1):91-102.e4. doi: 10.1016/j.neuron.2018.10.049. Epub 2018 Nov 21.

Higher-Order Thalamocortical Inputs Gate Synaptic Long-Term Potentiation via Disinhibition.

Author information

1
Department of Basic Neurosciences, Geneva University Neurocenter, Faculty of Medicine, University of Geneva, Geneva 1206, Switzerland.
2
Department of Basic Neurosciences, Geneva University Neurocenter, Faculty of Medicine, University of Geneva, Geneva 1206, Switzerland. Electronic address: anthony.holtmaat@unige.ch.

Abstract

Sensory experience and perceptual learning changes receptive field properties of cortical pyramidal neurons (PNs), largely mediated by synaptic long-term potentiation (LTP). The circuit mechanisms underlying cortical LTP remain unclear. In the mouse somatosensory cortex, LTP can be elicited in layer 2/3 PNs by rhythmic whisker stimulation. We dissected the synaptic circuitry underlying this type of plasticity in thalamocortical slices. We found that projections from higher-order, posterior medial thalamic complex (POm) are key to eliciting N-methyl-D-aspartate receptor (NMDAR)-dependent LTP of intracortical synapses. Paired activation of cortical and higher-order thalamocortical inputs increased vasoactive intestinal peptide (VIP) and parvalbumin (PV) interneuron (IN) activity and decreased somatostatin (SST) IN activity, which together disinhibited the PNs. VIP IN-mediated disinhibition was critical for inducing LTP. This study reveals a circuit motif in which higher-order thalamic inputs gate synaptic plasticity via disinhibition. This motif may allow contextual feedback to shape synaptic circuits that process first-order sensory information.

KEYWORDS:

POm; PV; SST; VIP; barrel cortex BC; disinhibition; long-term potentiation LTP; parvalbumin-expressing interneurons; plasticity; posterior medial complex of the thalamus; somatosensory; somatostatin-expressing interneurons; thalamus; vasoactive-intestinal-peptide-expressing interneurons

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