Kandasamy S B, Williams B A
Neuropharmacology. 1984 Jan;23(1):49-53. doi: 10.1016/0028-3908(84)90216-8.
Intracerebroventricular administration of adrenocorticotropin (ACTH 1-24) and alpha-melanotropin (alpha-MSH), peptides which occur naturally in brain induced dose-related hypothermia in guinea-pigs at room temperature (21 degrees C) and also produced greater hypothermia at low (10 degrees C) ambient temperature. However, when the experiments were repeated in a warm (30 degrees C) environment, no effect on body temperature was observed. These results indicate that the peptides did not reduce the central set-point of temperature control. The hypothermia induced by ACTH and alpha-MSH was not mediated via histamine H1- or H2-receptors and serotonin since the H1-receptor antagonist, mepyramine, the H2-receptor antagonist, cimetidine, and the serotonin antagonist, methysergide, had no antagonistic effects. The peptides were antipyretic since they reduced pyrogen-induced-fever and hyperthermia due to prostaglandin E2, norepinephrine and dibutyryl cAMP, at a dose which did not affect normal body temperature. The powerful central effects of these peptides on normal body temperature, fever and hyperthermia, together with their presence of the brain regions important to temperature control, suggest that they participate in thermoregulation.
在豚鼠脑室内注射促肾上腺皮质激素（ACTH 1-24）和α-促黑素（α-MSH），这两种在脑内天然存在的肽在室温（21摄氏度）下可诱导豚鼠出现剂量相关的体温过低，并且在低温（10摄氏度）环境下会产生更明显的体温过低。然而，当在温暖（30摄氏度）环境中重复这些实验时，未观察到对体温有任何影响。这些结果表明，这些肽并未降低体温控制的中枢设定点。促肾上腺皮质激素和α-促黑素诱导的体温过低不是通过组胺H1或H2受体以及5-羟色胺介导的，因为H1受体拮抗剂美吡拉敏、H2受体拮抗剂西咪替丁和5-羟色胺拮抗剂麦角新碱均无拮抗作用。这些肽具有解热作用，因为它们在不影响正常体温的剂量下，可降低由致热原引起的发热以及因前列腺素E2、去甲肾上腺素和二丁酰环磷腺苷导致的体温过高。这些肽对正常体温、发热和体温过高具有强大的中枢作用，再加上它们在对体温控制至关重要的脑区中存在，表明它们参与体温调节。
