Choe K Y, Trudel E, Bourque C W
Centre for Research in Neuroscience, Research Institute of the McGill University Health Centre, Montreal, Canada.
J Neuroendocrinol. 2016 Apr;28(4). doi: 10.1111/jne.12372.
Synaptic and extrasynaptic transmission mediated by ionotropic GABA and glycine receptors plays a critical role in shaping the action potential firing (spiking) activity of hypothalamic magnocellular neurosecretory cells and therefore determines the rate at which vasopressin and oxytocin are released from the neurohypophysis. The inhibitory effect of these transmitters relies on the maintenance of a low concentration of intracellular chloride ions such that, when activated by GABA or glycine, a hyperpolarisation of the neuronal membrane potential results. In this review, we highlight the various ways by which the two types of inhibitory receptors contribute to homeostasis by fine-tuning the spiking rate of vasopressin-releasing magnocellular neurosecretory cells in a manner dependent on the hydration state of the animal. In addition, we review the currently available evidence on how the strength of these inhibitory pathways can be regulated during chronic hypernatraemia via a form of activity-dependent depolarisation of the chloride reversal potential, leading to an abolition of these inhibitory pathways potentially causing sodium-dependent elevations in blood pressure.
由离子型γ-氨基丁酸（GABA）和甘氨酸受体介导的突触和突触外传递，在塑造下丘脑大细胞神经分泌细胞的动作电位发放（峰电位）活动中起关键作用，因此决定了血管加压素和催产素从神经垂体释放的速率。这些递质的抑制作用依赖于细胞内氯离子低浓度的维持，使得当被GABA或甘氨酸激活时，神经元膜电位会发生超极化。在这篇综述中，我们强调了这两种抑制性受体通过以依赖于动物水合状态的方式微调释放血管加压素的大细胞神经分泌细胞的峰电位发放速率，从而对体内平衡做出贡献的各种方式。此外，我们回顾了目前关于在慢性高钠血症期间，这些抑制性通路的强度如何通过氯离子反转电位的一种活动依赖性去极化形式进行调节的证据，这会导致这些抑制性通路的废除，可能引起血压的钠依赖性升高。
