Effects of General Anesthetics on Synaptic Transmission and Plasticity.
Effects of General Anesthetics on Synaptic Transmission and Plasticity.
复制标题
DOI：
10.2174/1570159x19666210803105232
复制
发表时间：
2022
影响因子：
5.3
通讯作者：
中科院分区：
文献类型：
--
作者：
全身麻醉药主要通过相对麻醉剂特异性机制分别调节谷氨酸能或 GABA 能突触的功能来抑制兴奋性和/或增强抑制性突触传递。突触信号蛋白（包括配体门控离子通道和电压门控离子通道）是全身麻醉剂的靶标，可调节各种突触机制，包括突触前神经递质释放、突触后受体信号传导和树突棘动力学，以产生其特有的急性神经生理学效应。由于突触结构和可塑性介导学习和记忆等高阶功能，麻醉后的长期突触功能障碍可能会导致不良的神经认知后果，具体取决于特定的麻醉剂和人群的脆弱性。在这里，我们回顾了突触传递和可塑性的短暂和持续全身麻醉改变的细胞和分子机制。
General anesthetics depress excitatory and/or enhance inhibitory synaptic transmission principally by modulating the function of glutamatergic or GABAergic synapses, respectively, with relative anesthetic agent-specific mechanisms. Synaptic signaling proteins, including ligand- and voltage-gated ion channels, are targeted by general anesthetics to modulate various synaptic mechanisms, including presynaptic neurotransmitter release, postsynaptic receptor signaling, and dendritic spine dynamics to produce their characteristic acute neurophysiological effects. As synaptic structure and plasticity mediate higher-order functions such as learning and memory, long-term synaptic dysfunction following anesthesia may lead to undesirable neurocognitive consequences depending on the specific anesthetic agent and the vulnerability of the population. Here we review the cellular and molecular mechanisms of transient and persistent general anesthetic alterations of synaptic transmission and plasticity.
影响因子：
4.7
作者：
Westphalen RI;Yu J;Krivitski M;Jih TY;Hemmings HC Jr
通讯作者：
Hemmings HC Jr
影响因子：
5.7
作者：
Zhang Y;Sharma M;Eger EI 2nd;Laster MJ;Hemmings HC Jr;Harris RA
通讯作者：
Harris RA