title: Synaptic plasticity at intrathalamic connections via CaV3.3 T-type Ca2+ channels and GluN2B-containing NMDA receptors.
abstract: 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.
authors.affiliation: Department of Fundamental Neurosciences, University of Lausanne, CH-1005 Lausanne, Switzerland. simone.astori@unil.ch
authors.forename: Simone
authors.initials: S
authors.lastname: Astori
authors.forename: Anita
authors.initials: A
authors.lastname: Lüthi
mesh_terms: D000818:Animals; D020747:Calcium Channels, T-Type / Q000235:genetics / Q000502:physiology*; D055724:Electrophysiological Phenomena; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D066298:In Vitro Techniques; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009473:Neuronal Plasticity / Q000235:genetics / Q000502:physiology*; D018091:Receptors, AMPA / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics / Q000502:physiology*; D012154:Reticular Formation / Q000254:growth & development / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology; D013788:Thalamus / Q000254:growth & development / Q000502:physiology*
chemical_list: C534770:Cacna1i protein, mouse; D020747:Calcium Channels, T-Type; C121001:NR2B NMDA receptor; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate