Specific GABAA circuits for visual cortical plasticity
Specific GABAA circuits for visual cortical plasticity
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DOI：
10.1126/science.1091032
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发表时间：
2004-03-12
期刊：
影响因子：
56.9
通讯作者：
Hensch, TK
中科院分区：
文献类型：
--
作者：
Fagiolini, M;Fritschy, JM;Hensch, TK
在生命早期，视觉皮质内的微弱抑制阻止了依赖经验的可塑性。通过用苯二氮类药物增强伽马氨基丁酸(GABA)介导的传递，可以过早地启动对失明眼睛的反应性丧失。在这里，我们使用小鼠对阿尔法亚基的“敲门”突变，使单个A型GABA(GABA(A))受体对安定不敏感，以表明特定的抑制网络控制关键期的表达。只有含有α1的回路才能驱动皮质的可塑性，而富含α2的连接则单独调节神经元。戒指。这种解离对大脑发育模型和用于婴儿的苯二氮卓类药物的安全设计具有重要意义。
Weak inhibition within visual cortex early in life prevents experience-dependent plasticity. Loss of responsiveness to an eye deprived of vision can be initiated prematurely by enhancing gamma-aminobutyric acid (GABA)-mediated transmission with benzodiazepines. Here, we use a mouse "knockin" mutation to alpha subunits that renders individual GABA type A(GABA(A)) receptors insensitive to diazepam to show that a particular inhibitory network controls expression of the critical period. Only alpha1-containing circuits were found to drive cortical plasticity, whereas alpha2-enriched connections separately regulated neuronal. ring. This dissociation carries implications for models of brain development and the safe design of benzodiazepines for use in infants.