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

First Author  Astori S Year  2013
Journal  J Neurosci Volume  33
Issue  2 Pages  624-30
PubMed ID  23303941 Mgi Jnum  J:318154
Mgi Id  MGI:6858490 Doi  10.1523/JNEUROSCI.3185-12.2013
Citation  Astori S, et al. (2013) Synaptic plasticity at intrathalamic connections via CaV3.3 T-type Ca2+ channels and GluN2B-containing NMDA receptors. J Neurosci 33(2):624-30
abstractText  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.
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