Effects of Salt Loading on the Regulation of Rat Hypothalamic Magnocellular Neurosecretory Cells by Ionotropic GABA and Glycine Receptors

被引:11
作者
Choe, K. Y. [1 ,2 ]
Trudel, E. [1 ]
Bourque, C. W. [1 ]
机构
[1] McGill Univ, Ctr Res Neurosci, Res Inst, Ctr Hlth, Montreal, PQ H3A 2T5, Canada
[2] Univ Calif Los Angeles, Dept Neurol, Gonda Neurosci & Genet Res Ctr 2309, 695 Charles E Young Dr South, Los Angeles, CA 90095 USA
基金
加拿大健康研究院;
关键词
supraoptic nucleus; vasopressin; oxytocin; GABA; glycine; osmolality; inhibition; salt loading; baroreceptor; arterial pressure; brain-derived neurotrophic factor; TrkB receptor; KCC2; chloride; GAMMA-AMINOBUTYRIC-ACID; FACTOR MESSENGER-RNA; K+-CL-COTRANSPORTER; SUPRAOPTIC VASOPRESSIN NEURONS; CATION-CHLORIDE-COTRANSPORTERS; VASCULOSUM LAMINA TERMINALIS; HIPPOCAMPAL NETWORK ACTIVITY; MEDIATED DOWN-REGULATION; NEUROTROPHIC FACTOR; LOCUS-COERULEUS;
D O I
10.1111/jne.12372
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
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页数:13
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