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外侧臂旁核5-羟色胺能机制与钠缺乏诱导的盐食欲

Lateral parabrachial nucleus serotonergic mechanisms and salt appetite induced by sodium depletion.

作者信息

Menani J V, De Luca L A, Johnson A K

机构信息

Department of Physiology, School of Dentistry, Paulista State University, Araraquara, Säo Paulo, Brazil.

出版信息

Am J Physiol. 1998 Feb;274(2 Pt 2):R555-60. doi: 10.1152/ajpregu.1998.274.2.r555.

Abstract

This study investigated the effects of bilateral injections of a serotonin (5-HT) receptor agonist into the lateral parabrachial nucleus (LPBN) on the intake of NaCl and water induced by 24-h water deprivation or by sodium depletion followed by 24 h of sodium deprivation (injection of the diuretic furosemide plus 24 h of sodium-deficient diet). Rats had stainless steel cannulas implanted bilaterally into the LPBN. Bilateral LPBN injections of the serotonergic 5-HT1/2 receptor antagonist methysergide (4 micrograms/200 nl at each site) increased hypertonic NaCl intake when tested 24 h after sodium depletion and after 24 h of water deprivation. Water intake also increased after bilateral injections of methysergide into the LPBN. In contrast, the intake of a palatable solution (0.06 M sucrose) under body fluid-replete conditions was not changed after bilateral LPBN methysergide injections. The results show that serotonergic mechanisms in the LPBN modulate water and sodium intake induced by volume depletion and sodium loss. The finding that sucrose intake was not affected by LPBN serotonergic blockade suggests that the effects of the methysergide treatment on the intakes of water and NaCl are not due to a mechanism producing a nonspecific enhancement of all ingestive behaviors.

摘要

本研究调查了向双侧臂旁外侧核(LPBN)注射5-羟色胺(5-HT)受体激动剂对因24小时禁水或因排钠继以24小时缺钠(注射利尿剂速尿加24小时低钠饮食)所诱导的氯化钠和水摄入的影响。大鼠双侧植入了通向LPBN的不锈钢套管。在缺钠24小时及禁水24小时后进行测试时,双侧LPBN注射5-羟色胺能5-HT1/2受体拮抗剂麦角酰二乙胺(每个位点4微克/200纳升)会增加高渗氯化钠的摄入量。向LPBN双侧注射麦角酰二乙胺后水的摄入量也增加。相比之下,在体液充足条件下给予可口溶液(0.06M蔗糖)时,双侧LPBN注射麦角酰二乙胺后其摄入量未发生变化。结果表明,LPBN中的5-羟色胺能机制可调节因容量耗竭和钠丢失所诱导的水和钠的摄入。麦角酰二乙胺处理对水和氯化钠摄入量有影响,但对蔗糖摄入量无影响,这一发现表明,麦角酰二乙胺处理对水和氯化钠摄入量的影响并非由于一种能非特异性增强所有摄食行为的机制所致。

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