缝隙连接蛋白 36 形成的电突触调节抑制作用和经验依赖性可塑性。
Electrical synapses formed by connexin36 regulate inhibition- and experience-dependent plasticity.
机构信息
Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
出版信息
Proc Natl Acad Sci U S A. 2011 Aug 16;108(33):13770-5. doi: 10.1073/pnas.1100166108. Epub 2011 Jul 29.
Abstract
The mammalian brain constantly adapts to new experiences of the environment, and inhibitory circuits play a crucial role in this experience-dependent plasticity. A characteristic feature of inhibitory neurons is the establishment of electrical synapses, but the function of electrical coupling in plasticity is unclear. Here we show that elimination of electrical synapses formed by connexin36 altered inhibitory efficacy and caused frequency facilitation of inhibition consistent with a decreased GABA release in the inhibitory network. The altered inhibitory efficacy was paralleled by a failure of theta-burst long-term potentiation induction and by impaired ocular dominance plasticity in the visual cortex. Together, these data suggest a unique mechanism for regulating plasticity in the visual cortex involving synchronization of inhibitory networks via electrical synapses.
摘要
哺乳动物大脑不断适应环境的新体验，而抑制性回路在这种经验依赖性可塑性中起着至关重要的作用。抑制性神经元的一个特征是建立电突触，但电耦合在可塑性中的功能尚不清楚。在这里，我们表明，消除连接蛋白 36 形成的电突触会改变抑制效能，并导致抑制的频率促进，这与抑制性网络中 GABA 释放减少一致。抑制效能的改变伴随着θ爆发长时程增强诱导的失败和视觉皮层中眼优势可塑性的受损。总的来说，这些数据表明了一种独特的机制，可以通过电突触来调节视觉皮层中的可塑性，涉及抑制性网络的同步。
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