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喹哌嗪通过激活5-羟色胺2受体来减少大鼠的食物摄入量。

Quipazine reduces food intake in the rat by activation of 5-HT2-receptors.

作者信息

Hewson G, Leighton G E, Hill R G, Hughes J

机构信息

Parke-Davis Research Unit, Addenbrookes Hospital Site, Cambridge.

出版信息

Br J Pharmacol. 1988 Oct;95(2):598-604. doi: 10.1111/j.1476-5381.1988.tb11681.x.

Abstract
  1. To determine which subtype(s) of 5-hydroxytryptamine (5-HT) receptor are involved in the anorectic action of quipazine, the ability of selective antagonists at 5-HT2- and 5-HT3-receptors, and an antagonist at 5-HT1-like receptors, to block this response were investigated in non-deprived rats, trained to eat a palatable diet. 2. Quipazine (0.5-8 mg kg-1, i.p.) produced a dose-related reduction in the intake of palatable diet. 3. The anorectic effect of 4 mg kg-1 quipazine was antagonized by the nonselective 5-HT-receptor antagonist methysergide (5 mg kg-1, i.p.) and by the selective 5-HT2-receptor antagonists ketanserin (1 mg kg-1 and 2.5 mg kg-1, i.p.) and ritanserin (0.5 mg kg-1 and 1 mg kg-1, i.p.). The selective 5-HT3-receptor antagonist GR38032F (1 mg kg-1, i.p.) and (-)-pindolol (4 mg kg-1, i.p.), which blocks some of the effects mediated at 5-HT1-like receptors, did not block the reduction in food intake produced by this dose of quipazine. 4. None of the 5-HT-receptor antagonists had any effect on food intake when they were administered alone, suggesting that endogenous 5-HT is not involved in the tonic control of food intake under the conditions of these experiments. 5. It is concluded that the anorectic action of quipazine is mediated, at least in part, by activation of 5-HT2-receptors.
摘要
  1. 为了确定5-羟色胺(5-HT)受体的哪些亚型参与了喹哌嗪的厌食作用,在训练以食用美味食物的非饥饿大鼠中,研究了5-HT2和5-HT3受体选择性拮抗剂以及5-HT1类受体拮抗剂阻断这种反应的能力。2. 喹哌嗪(0.5 - 8毫克/千克,腹腔注射)使美味食物的摄入量产生剂量相关的减少。3. 4毫克/千克喹哌嗪的厌食作用被非选择性5-HT受体拮抗剂美西麦角(5毫克/千克,腹腔注射)以及选择性5-HT2受体拮抗剂酮色林(1毫克/千克和2.5毫克/千克,腹腔注射)和利坦色林(0.5毫克/千克和1毫克/千克,腹腔注射)所拮抗。选择性5-HT3受体拮抗剂GR38032F(1毫克/千克,腹腔注射)和(-)-吲哚洛尔(4毫克/千克,腹腔注射),后者可阻断一些由5-HT1类受体介导的效应,并未阻断该剂量喹哌嗪引起的食物摄入量减少。4. 当单独给予时,这些5-HT受体拮抗剂均对食物摄入量没有任何影响,这表明在这些实验条件下内源性5-HT不参与食物摄入的紧张性控制。5. 得出的结论是,喹哌嗪的厌食作用至少部分是由5-HT2受体的激活介导的。

相似文献

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Evidence for 5-HT2 receptor mediation in quipazine anorexia.
Psychopharmacology (Berl). 1990;100(1):115-8. doi: 10.1007/BF02245800.

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