Tasker Jeffrey G, Di Shi, Boudaba Cherif
Department of Cell and Molecular Biology, Neurobiology Division, 2000 Percival Stern Hall, Tulane University, New Orleans, LA 70118, USA.
Prog Brain Res. 2002;139:113-9. doi: 10.1016/s0079-6123(02)39011-3.
The hypothalamic-neurohypophysial system undergoes dramatic morphological plasticity in response to physiological activation during parturition/lactation and dehydration, including somatic swelling, decreased glial coverage and increased synaptic innervation of the magnocellular neuroendocrine cells. Recent in-vitro electrophysiological studies in hypothalamic slices have demonstrated that coordinate changes in the synaptic physiology of the magnocellular neurons also occur under these conditions. Thus, the synaptic release of glutamate and GABA onto magnocellular neurons is increased during lactation and with chronic dehydration, and changes in postsynaptic glutamate and GABAA receptor expression lead to alterations of the functional properties of the glutamate and GABAA receptor channels. The presynaptic noradrenergic facilitation of glutamate release and inhibition of GABA release is also markedly enhanced following chronic dehydration. Additionally, both parturition and chronic dehydration are accompanied by an increase in the tonic activation of presynaptic metabotropic glutamate receptors due to the higher ambient glutamate concentration caused by decreased glial coverage and the resultant reduction in glutamate reuptake. Together, these electrophysiological studies reveal profound functional plasticity in the synaptic physiology of magnocellular neurons at parturition and following dehydration. The plastic changes support an increase in the excitability of magnocellular neuroendocrine cells by increasing glutamate inputs, decreasing GABA inputs, enhancing excitatory noradrenergic modulation, and reducing synaptic glutamatergic noise.
下丘脑 - 神经垂体系统在分娩/哺乳和脱水等生理激活过程中会经历显著的形态可塑性变化，包括体细胞肿胀、神经胶质覆盖减少以及大细胞神经内分泌细胞的突触支配增加。最近在下丘脑切片上进行的体外电生理研究表明，在这些条件下，大细胞神经元的突触生理学也会发生协同变化。因此，在哺乳期间和长期脱水时，谷氨酸和GABA向大细胞神经元的突触释放会增加，并且突触后谷氨酸和GABAA受体表达的变化会导致谷氨酸和GABAA受体通道功能特性的改变。长期脱水后，去甲肾上腺素能对谷氨酸释放的突触前促进作用和对GABA释放的抑制作用也会显著增强。此外，由于神经胶质覆盖减少导致细胞外谷氨酸浓度升高以及由此引起的谷氨酸再摄取减少，分娩和长期脱水都会伴随着突触前代谢型谷氨酸受体的紧张性激活增加。总之，这些电生理研究揭示了分娩时和脱水后大细胞神经元突触生理学中深刻的功能可塑性。这些可塑性变化通过增加谷氨酸输入、减少GABA输入、增强兴奋性去甲肾上腺素能调制以及减少突触谷氨酸能噪声来支持大细胞神经内分泌细胞兴奋性的增加。
