Neural input modulates osmotically stimulated release of vasopressin into the supraoptic nucleus.
Neural input modulates osmotically stimulated release of vasopressin into the supraoptic nucleus.
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神经输入调节渗透刺激的加压素释放到视上核。
DOI：
10.1152/ajpendo.1996.270.5.e787
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Morris,M
中科院分区：
文献类型：
--
作者：
Ludwig,M;Callahan,MF;Landgraf,R;Johnson,AK;Morris,M
确定了第三脑室前腹侧 (AV3V) 区域的损伤对中枢和全身渗透刺激反应中加压素 (VP) 释放到视上核 (SON) 和血液中的影响。将微透析探针植入具有假手术或 AV3V 损伤的雄性尿烷麻醉大鼠的 SON 内。腹膜内给予渗透刺激（3.5 M 氯化钠，600微升/100克体重），然后通过微透析探针（1 M 氯化钠-人工脑脊液）。 AV3V 损伤减弱了对全身渗透刺激的反应。病变大鼠对腹膜内 NaCl 的核内 VP 释放没有增加，血浆 VP 减少（增加 42.6 +/- 8.4 vs. 78.0 +/- 16.4 pg/ml）和血压反应（7.1 +/- 2.3 vs. 19.6 +/- 3.2 mmHg）。相比之下，内分泌和心血管对细胞核直接渗透刺激的反应如之前的研究所示，并且似乎不受病变的影响。这些结果表明，AV3V 区域的损伤会中断神经元输入，从而触发垂体后叶分泌 VP 并释放到 SON 的细胞外室中。
The effects of lesioning of the anteroventral third ventricle (AV3V) region on vasopressin (VP) release into the supraoptic nucleus (SON) and blood in response to central and systemic osmotic stimulation were determined. Microdialysis probes were implanted bilaterally within the SON of male urethan-anesthetized rats with sham or AV3V lesions. Osmotic stimuli were administered intraperitoneally (3.5 M NaCl, 600 microliters/100 g body wt) and then via the microdialysis probes (1 M NaCl-artificial cerebrospinal fluid). AV3V lesions attenuated the response to systemic osmotic stimulation. The lesioned rats showed no increase in intranuclear VP release and reduced plasma VP (increase of 42.6 +/- 8.4 vs. 78.0 +/- 16.4 pg/ml) and blood pressure responses (7.1 +/- 2.3 vs. 19.6 +/- 3.2 mmHg) to intraperitoneal NaCl. In contrast, the endocrine and cardiovascular responses to direct osmotic stimulation of the nucleus were as seen in previous studies and seemed to be unaffected by the lesion. These results show that lesion of the AV3V region interrupts neuronal inputs which trigger VP secretion from the posterior pituitary as well as release into the extracellular compartment of the SON.