Connexin 43 Modulates Regulated Exocytosis

摘要 星形胶质细胞-神经元信号，又名。神经胶质传递，可调节突触传递/可塑性 三方突触。神经胶质传递调节的过程包括睡眠调节、呼吸和 学习/记忆。尽管胶质传递在这些基本的生命过程中扮演了这些角色，但它的机制是 我不明白。阐明这一机制应该能提供对基本大脑过程的见解，并提示 当他们出了问题时进行干预。两项关于星形胶质细胞-神经元信号的早期研究探索了这一假设 星形细胞谷氨酸释放作用于神经元谷氨酸受体，但他们得出了不同的结论 关于这一机制。一项研究得出结论，谷氨酸不是信使，而是建议 这种缝隙连接可能参与星形胶质细胞-神经元信号的传递。另一项研究得出结论，信号是 由依赖于钙的星形胶质细胞释放谷氨酸介导，随后被证明是通过调节 含谷氨酸的囊泡的胞吐作用。人们对亚细胞的了解几乎一无所知。 星形胶质细胞释放部位的分布/定位。目前还不清楚它们是否唯一地局限于三方 星形胶质细胞或更广泛的突触区域。关于胞吐作用和细胞外排出作用的相对作用有很大的争论。 缝隙连接介导的通讯是星形胶质细胞-神经元信号的关键。我们的初步数据显示 新的、统一的假设认为，这两种机制实际上是机械联系的。

Abstract Astrocyte-neuron signaling, a.k.a. gliotransmission, can modulate synaptic transmission/plasticity at tripartite synapses. Among the processes regulated by gliotransmission are sleep-regulation, respiration, and learning/memory. Despite these roles of gliotransmission in such fundamental life processes, its mechanism is not understood. Elucidating this mechanism should provide insights into basic brain processes, and suggest interventions when they go awry. Two early studies of astrocyte-neuron signaling explored the hypothesis that astrocytic glutamate release acts on neuronal glutamate receptors, but they led to different conclusions regarding the mechanism. One study concluded that glutamate is not the messenger but instead suggested that gap junctions might mediate astrocyte-neuron signaling. The other study concluded that the signaling is mediated by Ca2+-dependent glutamate release from astrocytes, subsequently shown to occur by regulated exocytosis of glutamate-containing vesicles. Virtually nothing is known about the subcellular distribution/localization of astrocyte release sites. It is not clear if they are localized uniquely to the tripartite synaptic regions of astrocytes or more broadly. There is much debate about the relative roles of exocytosis vs. gap junction-mediated communication as critical for astrocyte-neuron signals. Our preliminary data point to a novel, unifying hypothesis that these two mechanisms are, in fact, mechanistically linked.