Amir S, Schiavetto A
Department of Psychology, Concordia University, Montreal, Que, Canada.
Brain Res. 1990 Sep 24;528(1):138-42. doi: 10.1016/0006-8993(90)90206-q.
E series prostaglandins (PGE) are known to elicit potent hyperthermia when injected into the anterior hypothalamic preoptic area (POAH) in rats, but the effector mechanisms mediating the rise in temperature are not well defined. In the present study, microinjection of PGE2 into the POAH dose-dependently increased non-shivering thermogenesis in brown adipose tissue (BAT) in urethananesthetized rats, bringing about a marked and sustained rise in interscapular BAT (IBAT) and core temperatures. The effect of intra-POAH PGE2 injection on IBAT and core temperatures could be blocked by systemic pretreatment with the sympathetic ganglionic blocker chlorisondamine chloride or the beta-adrenergic receptor blocker propranolol, thus implicating the involvement of the sympathetic system. Furthermore, the increase in IBAT and core temperatures induced by intra-POAH PGE2 could be blocked by prior injection of the local anesthetic procaine or the GABA receptor agonist muscimol into the ipsilateral ventromedial hypothalamic nucleus (VMH). Taken together, the results suggest that PGE2 increases body temperature by acting in the POAH to stimulate heat production in BAT via a sympathetic efferent mechanism located in the VMH.
已知E系列前列腺素（PGE）注入大鼠下丘脑视前区前部（POAH）时会引发强烈的体温过高，但介导体温升高的效应机制尚未明确。在本研究中，向POAH微量注射PGE2可使乌拉坦麻醉大鼠的棕色脂肪组织（BAT）非颤抖性产热呈剂量依赖性增加，导致肩胛间BAT（IBAT）和核心体温显著且持续升高。向POAH内注射PGE2对IBAT和核心体温的影响可被交感神经节阻滞剂氯异吲哚铵或β-肾上腺素能受体阻滞剂普萘洛尔全身预处理所阻断，因此表明交感神经系统参与其中。此外，POAH内注射PGE2所诱导的IBAT和核心体温升高可被事先向同侧腹内侧下丘脑核（VMH）注射局部麻醉药普鲁卡因或GABA受体激动剂蝇蕈醇所阻断。综上所述，结果表明PGE2通过作用于POAH，经由位于VMH的交感传出机制刺激BAT产热来升高体温。
