Advances in the neurophysiology of magnocellular neuroendocrine cells.
Advances in the neurophysiology of magnocellular neuroendocrine cells.
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大细胞神经内分泌细胞的神经生理学进展。
DOI：
10.1111/jne.12826
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发表时间：
2020
影响因子：
3.2
通讯作者：
Amstrong,WilliamE
中科院分区：
文献类型：
--
作者：
Tasker,JeffreyG;Prager-Khoutorsky,Masha;Teruyama,Ryoichi;Lemos,JoséR;Amstrong,WilliamE
下丘脑大细胞神经内分泌细胞具有独特的电特性和显著的形态和突触可塑性。它们庞大的躯体尺寸，它们在视上核和室旁核中相对均匀和密集的聚集，以及它们在神经垂体中的大轴突末梢，使它们成为直接电生理询问的有吸引力的目标。在这里，我们简要回顾了这些神经元的神经可塑性和神经生理学特性的重要最新发现，这些发现是在2019年4月在以色列艾因盖迪举行的第13届世界神经垂体激素大会期间的研讨会“大细胞神经元电生理学”上提出的。大细胞血管加压素（VP）神经元直接对高渗刺激产生反应，引起膜去极化，这是由细胞收缩诱导的瞬时受体电位香草酸1型（TRPV 1）通道的N末端截短变体开放触发的。新的发现表明，这种机械转导依赖于肌动蛋白和微管细胞骨架网络，TRPV 1通道与微管的直接偶联是通道机械门控的原因。加压素神经元也通过激活上皮Na+通道（ENaC）对血管紧张素Ⅱ刺激作出反应。最近的研究表明，ENaC活性的变化通过产生膜电位的紧张性变化来调节大细胞神经元的基础放电。催产素和VP神经元在慢性渗透刺激期间也经历强兴奋性突触可塑性。最近的研究结果表明，在慢性盐负荷过程中诱导的新谷氨酸突触表达高度不稳定的Ca 2+渗透性GluA 1受体，需要持续的树突蛋白合成来维持突触。最后，最近，来自独特易处理的神经垂体终末的记录揭示了活动依赖性神经肽释放的意想不到的特性。发现电压依赖性神经垂体神经分泌的显著部分不依赖于通过电压门控Ca 2+通道的Ca 2+内流。总之，这些发现提供了下丘脑-神经垂体系统的电生理信号机制和神经可塑性的重要新进展的快照，该系统继续为神经生理学领域做出重要贡献。
Hypothalamic magnocellular neuroendocrine cells have unique electrical properties and a remarkable capacity for morphological and synaptic plasticity. Their large somatic size, their relatively uniform and dense clustering in the supraoptic and paraventricular nuclei, and their large axon terminals in the neurohypophysis make them an attractive target for direct electrophysiological interrogation. Here, we provide a brief review of significant recent findings in the neuroplasticity and neurophysiological properties of these neurones that were presented at the symposium “Electrophysiology of Magnocellular Neurons” during the 13th World Congress on Neurohypophysial Hormones in Ein Gedi, Israel in April 2019. Magnocellular vasopressin (VP) neurones respond directly to hypertonic stimulation with membrane depolarisation, which is triggered by cell shrinkage‐induced opening of an N‐terminal‐truncated variant of transient receptor potential vanilloid type‐1 (TRPV1) channels. New findings indicate that this mechanotransduction depends on actin and microtubule cytoskeletal networks, and that direct coupling of the TRPV1 channels to microtubules is responsible for mechanical gating of the channels. Vasopressin neurones also respond to osmostimulation by activation of epithelial Na+channels (ENaC). It was shown recently that changes in ENaC activity modulate magnocellular neurone basal firing by generating tonic changes in membrane potential. Both oxytocin and VP neurones also undergo robust excitatory synapse plasticity during chronic osmotic stimulation. Recent findings indicate that new glutamate synapses induced during chronic salt loading express highly labile Ca2+‐permeable GluA1 receptors requiring continuous dendritic protein synthesis for synapse maintenance. Finally, recordings from the uniquely tractable neurohypophysial terminals recently revealed an unexpected property of activity‐dependent neuropeptide release. A significant fraction of the voltage‐dependent neurohypophysial neurosecretion was found to be independent of Ca2+influx through voltage‐gated Ca2+channels. Together, these findings provide a snapshot of significant new advances in the electrophysiological signalling mechanisms and neuroplasticity of the hypothalamic‐neurohypophysial system, a system that continues to make important contributions to the field of neurophysiology.