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The T-type Ca(2+) channels encoded by the Ca(V)3 genes are well established electrogenic drivers for burst discharge. Here, using Ca(V)3.3(-/-) mice we found that Ca(V)3.3 channels trigger synaptic plasticity in reticular thalamic neurons. Burst discharge via Ca(V)3.3 channels induced long-term potentiation at thalamoreticular inputs when coactivated with GluN2B-containing NMDA receptors, which are the dominant subtype at these synapses. Notably, oscillatory burst discharge of reticular neurons is typical for sleep-related rhythms, suggesting that sleep contributes to strengthening intrathalamic circuits.

Synaptic Plasticity at Intrathalamic Connections via CaV3.3 T-type Ca2+Channels and GluN2B-Containing NMDA Receptors

Synaptic Plasticity at Intrathalamic Connections via Ca_V3.3 T-type Ca²⁺Channels and GluN2B-Containing NMDA Receptors