Synaptic plasticity at intrathalamic connections via CaV3.3 T-type Ca2+ channels and GluN2B-containing NMDA receptors

Abstract

The T-type Ca2+ channels encoded by the CaV3 genes are well established electrogenic drivers for burst discharge. Here, using CaV3.3-/- mice we found that CaV3.3 channels rigger synaptic plasticity in reticular thalamic neurons. Burst discharge via CaV3.3 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. © 2013 the authors.