Scientific article
Open access

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

Published inNeuron, vol. 101, no. 1, p. 91-102.e4
Publication date2019

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.

  • Plasticity
  • Long-term potentiation LTP
  • Thalamus
  • Somatosensory
  • Barrel cortex BC
  • Disinhibition
  • Posterior medial complex of the thalamus
  • POm
  • Somatostatin-expressing interneurons
  • SST
  • Vasoactive-intestinal-peptide-expressing interneurons
  • VIP
  • Parvalbumin-expressing interneurons
  • PV
Citation (ISO format)
WILLIAMS, Leena Eve, HOLTMAAT, Anthony. Higher-Order Thalamocortical Inputs Gate Synaptic Long-Term Potentiation via Disinhibition. In: Neuron, 2019, vol. 101, n° 1, p. 91–102.e4. doi: 10.1016/j.neuron.2018.10.049
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Article (Published version)
ISSN of the journal0896-6273

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