Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking α1G T-type Ca2+ channels
Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking α1G T-type Ca2+ channels
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DOI：
10.1016/s0896-6273(01)00343-9
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发表时间：
2001-07-19
期刊：
影响因子：
16.2
通讯作者：
Shin, HS
中科院分区：
文献类型：
--
作者：
Kim, D;Song, I;Shin, HS
T型钙电流已被提出参与棘波放电的发生，失神发作的迹象，但在体内的直接证据来支持这一假设一直缺乏。为了解决这个问题，我们产生了T型钙离子通道的α（1G）亚基的无效突变。α（1G）缺陷小鼠的丘脑皮质中继神经元缺乏动作电位的爆发模式放电，而它们显示出正常的强直模式放电模式。α（1G）缺乏的丘脑对GABA（B）受体激活产生的棘波放电具有特异性抗性。因此，α（1G）T型钙通道介导的内在放电模式的调制在丘脑皮质通路的失神发作的发生中起着关键作用。
T-type Ca2+ currents have been proposed to be involved in the genesis of spike-and-wave discharges, a sign of absence seizures, but direct evidence in vivo to support this hypothesis has been lacking. To address this question, we generated a null mutation of the alpha (1G) subunit of T-type Ca2+ channels. The thalamocortical relay neurons of the alpha (1G)-deficient mice lacked the burst mode firing of action potentials, whereas they showed the normal pattern of tonic mode firing. The alpha (1G)-deficient thalamus was specifically resistant to the generation of spike-and-wave discharges in response to GABA(B) receptor activation. Thus, the modulation of the intrinsic firing pattern mediated by alpha (1G) T-type Ca2+ channels plays a critical role in the genesis of absence seizures in the thalamocortical pathway.