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大鼠穹窿下器损伤可消除异丙肾上腺素和血清素的致渴作用。

Subfornical organ lesions in rats abolish hyperdipsic effects of isoproterenol and serotonin.

作者信息

Hubbard J I, Lin N, Sibbald J R

机构信息

Department of Physiology, University of Otago Medical School, Dunedin, New Zealand.

出版信息

Brain Res Bull. 1989 Jul-Aug;23(1-2):41-5. doi: 10.1016/0361-9230(89)90161-5.

Abstract

Isoproterenol (300 micrograms/ml/kg) and serotonin (2 mg/ml/kg) given SC to rats (n = 27) caused significant drinking (Fisher PLSD, Scheffe F test, Dunnett t) in the 1 and 2 hours after injection. Such drinking was completely prevented in rats later shown to have complete lesions of their subfornical organs (n = 7). In contrast a response not significantly different from the prelesion response was found in rats later given cortical lesions (n = 11) or other lesions which did not damage the subfornical organ (n = 7). We conclude that drinking evoked by SC injection of serotonin and isoproterenol is brought about by peripheral production of angiotensin II. Blood borne angiotensin II in turn stimulates neurons in subfornical organ which initiate the neural organization of a drinking response.

摘要

给大鼠(n = 27)皮下注射异丙肾上腺素(300微克/毫升/千克)和血清素(2毫克/毫升/千克),在注射后的1至2小时内引起显著饮水(Fisher PLSD、Scheffe F检验、Dunnett t检验)。后来发现有7只大鼠穹窿下器官完全受损,这些大鼠的这种饮水行为完全被阻止。相比之下,后来有11只大鼠接受了皮层损伤,或7只大鼠接受了其他未损伤穹窿下器官的损伤,这些大鼠的反应与损伤前的反应无显著差异。我们得出结论,皮下注射血清素和异丙肾上腺素引起的饮水是由外周产生的血管紧张素II导致的。血液循环中的血管紧张素II反过来刺激穹窿下器官中的神经元,从而启动饮水反应的神经机制。

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