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

被引：39
作者：
Astori, Simone [1 ]
Luethi, Anita [1 ]
机构：
[1] Univ Lausanne, Dept Fundamental Neurosci, CH-1005 Lausanne, Switzerland
来源：
JOURNAL OF NEUROSCIENCE | 2013年 / 33卷 / 02期
基金：
瑞士国家科学基金会;
关键词：
THALAMIC NEURONS; NUCLEUS-RETICULARIS; CALCIUM-CHANNELS; JUVENILE RATS; GRANULE CELLS; SLEEP; EXPRESSION; SYNAPSES; BRAIN; CURRENTS;
D O I：
10.1523/JNEUROSCI.3185-12.2013
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The T-type Ca2+ 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.
引用
收藏
页码：624 / 630
页数：7
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