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大鼠前列腺素E1发热期间的非寒战产热:大脑皮层的作用

Non-shivering thermogenesis during prostaglandin E1 fever in rats: role of the cerebral cortex.

作者信息

Monda M, Amaro S, De Luca B

机构信息

Department of Human Physiology, Faculty of Medicine and Surgery, Second University of Naples, Italy.

出版信息

Brain Res. 1994 Jul 18;651(1-2):148-54. doi: 10.1016/0006-8993(94)90691-2.

Abstract

We have tested the hypothesis that there is a role for the cerebral cortex in the control of non-shivering thermogenesis during fever induced by prostaglandin E1 (PGE1). While under urethan anesthesia, the firing rate of nerves innervating interscapular brown adipose tissue (IBAT), IBAT and colonic temperatures (TIBAT and Tc) and oxygen (O2) consumption were monitored during the fever from PGE1 injection (400 and 800 ng) in a lateral cerebral ventricle in controls and in functionally decorticated Sprague-Dawley rats. Rats were functionally decorticated by applying 3.3 M KCl solution on the frontal cortex which causes cortical spreading depression (CSD). Pyrogen injections caused dose-related increases in firing rate, TIBAT, Tc and O2 consumption and CSD reduced these enhancements. Our findings indicate that the cerebral cortex could be involved in the control of non-shivering thermogenesis during PGE1-induced febrile response.

摘要

我们检验了这样一个假设,即大脑皮层在前列腺素E1(PGE1)诱导发热期间对非寒战产热的控制中发挥作用。在乌拉坦麻醉下,监测了对照组和功能性去皮质的Sprague-Dawley大鼠在向侧脑室注射PGE1(400和800 ng)引起发热过程中,支配肩胛间棕色脂肪组织(IBAT)的神经放电频率、IBAT和结肠温度(TIBAT和Tc)以及氧气(O2)消耗情况。通过在额叶皮质应用3.3 M KCl溶液导致皮质扩散性抑制(CSD),使大鼠功能性去皮质。致热原注射导致放电频率、TIBAT、Tc和O2消耗呈剂量相关增加,而CSD降低了这些增强作用。我们的研究结果表明,大脑皮层可能参与了PGE1诱导的发热反应期间非寒战产热的控制。

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