Prostaglandins and hypothalamic neurotransmitter receptors involved in hyperthermia: a critical evaluation.
Prostaglandins and hypothalamic neurotransmitter receptors involved in hyperthermia: a critical evaluation.
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参与热疗的前列腺素和下丘脑神经递质受体：关键评估。
DOI：
10.1016/0149-7634(94)90033-7
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发表时间：
1994
影响因子：
8.2
通讯作者：
Myers,RD
中科院分区：
文献类型：
--
作者：
Simpson,CW;Ruwe,WD;Myers,RD
E系列前列腺素（PGE）在发热下丘脑机制中的作用仍有争议。本文回顾了历史文献和目前的研究结果的中心作用的PGEs对体温（Tb）。进行了新的实验，以检查毒蕈碱、烟碱、肾上腺素能、α-肾上腺素能或β-肾上腺素能受体拮抗剂在下丘脑部位的局部作用，在这些部位，PGE 1引起灵长类动物Tb 1升高。将用于显微注射的导管立体定位地植入雄性猕猴的下丘脑前部视前区（AH/POA）内和周围的部位上方。术后恢复后，在AH/POA区单侧微量注射前列腺素E130 -100 ng（1.0-1.5 μl），引起Tb升高，一旦确定，用受体拮抗剂预处理。在AH/POA的PGE 1反应位点微量注射毒蕈碱和烟碱拮抗剂阿托品或美加明，可显著降低PGE 1体温过高。在下丘脑腹内侧的PGE 1敏感部位注射孕酮能拮抗剂麦角新碱，也能减弱Tb的升高。然而，在AH/POA内注射5-HT再摄取阻断剂氟西汀和β-肾上腺素能受体拮抗剂普萘洛尔不能改变PGE 1的体温升高。相反，α-肾上腺素能受体拮抗剂酚妥拉明可增强下丘脑所有PGE 1反应位点Tbat的增加。一个更新的模型，以解释如何在下丘脑的胺能神经递质作用于各自的受体的并发行动可以与前列腺素E相互作用，引起体温过高。最后，对当前文献的评价，包括最近对巨噬细胞炎性蛋白（MIP-1）的研究结果，支持以下结论：脑中的PGE既不是热原性发热表达的强制性因素，也不是必要因素。
The role of a prostaglandin of the E series (PGE) in the hypothalamic mechanisms underlying a fever continues to be controversial. This paper reviews the historical literature and current findings on the central action of the PGEs on body temperature (Tb). New experiments were undertaken to examine the local effect of muscarinic, nicotinic, serotonergic, α-adrenergic, or β-adrenergic receptor antagonists at hypothalamic sites where PGE1caused a rise in Tbof the primate. Guide tubes for microinjection were implanted stereotaxically above sites in and around the anterior hypothalamic, preoptic area (AH/POA) of male Macaque monkeys. Following postoperative recovery, 30–100 ng of PGE1was micro-injected unilaterally in a volume of 1.0–1.5 μl at sites in the AH/POA to evoke a rise in Tb, and once identified, pretreated with a receptor antagonist. PGE1hyperthermia was significantly reduced by microinjections of the muscarinic and nicotinic antagonists, atropine, or mecamylamine, at PGE1reactive sites in the AH/POA. The serotonergic antagonist, methysergide, injected at PGE1sensitive sites in the ventromedial hypothalamus also attenuated the rise in Tb. However, the 5-HT reuptake blocker, fluoxetine, and the β-adrenergic receptor antagonist, propranolol, injected in the AH/POA failed to alter the PGE1hyperthermia. In contrast, the α-adrenergic antagonist, phentolamine, potentiated the increase in Tbat all PGE1reactive sites in the hypothalamus. An updated model is presented to explain how the concurrent actions of aminergic neurotransmitters acting on their respective receptors in the hypothalamus can interact with a PGE to elicit hyperthermia. Finally, an evaluation of the current literature including recent findings on macrophage inflammatory protein (MIP-1) supports the conclusion that a PGE in the brain is neither an obligatory nor essential factor for the expression of a pyrogen fever.