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

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Version: Author's accepted manuscript
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Version: author
Serval ID
serval:BIB_9D57B64D34E0
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Synaptic Plasticity at Intrathalamic Connections via CaV3.3 T-type Ca2+ Channels and GluN2B-Containing NMDA Receptors.
Journal
Journal of Neuroscience
Author(s)
Astori S., Lüthi A.
ISSN
1529-2401 (Electronic)
ISSN-L
0270-6474
Publication state
Published
Issued date
2013
Peer-reviewed
Oui
Volume
33
Number
2
Pages
624-630
Language
english
Notes
Publication types: Journal Article
pdf: Brief Communications
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.
Pubmed
Web of science
Open Access
Yes
Create date
21/01/2013 10:40
Last modification date
20/08/2019 15:03
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