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血管加压素在体内促进其自身于大鼠视上核中的释放。

Vasopressin facilitates its own release within the rat supraoptic nucleus in vivo.

作者信息

Wotjak C T, Ludwig M, Landgraf R

机构信息

Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany.

出版信息

Neuroreport. 1994 Jun 2;5(10):1181-4. doi: 10.1097/00001756-199406020-00005.

Abstract

A combined microdialysis/microinfusion technique was used to investigate whether arginine vasopressin (AVP) is involved in the regulation of its own release into the extracellular fluid of the supraoptic nucleus in vivo. While intranuclear neuropeptide release was monitored, 0.33 microliter of either vehicle, lysine vasopressin (LVP; 10 ng microliters -1) or a V1/V2 AVP receptor antagonist (100 ng microliters -1) was infused into the supraoptic nucleus of adult male Wistar rats before and during direct osmotic stimulation of the nucleus via the microdialysis probe. Administration of LVP increased basal AVP release, whereas administration of the V1/V2 receptor antagonist attenuated the increase in AVP release during osmotic stimulation observed in vehicle-treated controls. Taken together, these results indicate a receptor-mediated positive feedback action of endogenous AVP on its own release within the supraoptic nucleus.

摘要

采用微透析/微灌注联合技术研究精氨酸加压素(AVP)是否参与其自身向视上核细胞外液释放的体内调节。在监测核内神经肽释放的同时,在通过微透析探针对视上核进行直接渗透刺激之前和期间,将0.33微升的溶剂、赖氨酸加压素(LVP;10纳克/微升-1)或V1/V2 AVP受体拮抗剂(100纳克/微升-1)注入成年雄性Wistar大鼠的视上核。给予LVP增加了基础AVP释放,而给予V1/V2受体拮抗剂减弱了在溶剂处理对照组中观察到的渗透刺激期间AVP释放的增加。综上所述,这些结果表明内源性AVP在视上核内对其自身释放具有受体介导的正反馈作用。

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