Simansky K J
Department of Pharmacology, Medical College of Pennsylvania, Eastern Pennsylvania Psychiatric Institute, Philadelphia 19129.
Pharmacol Biochem Behav. 1991 Feb;38(2):459-62. doi: 10.1016/0091-3057(91)90306-m.
Subcutaneous administration of the prototypical 5-HT1-like agonist, 5-carboxamidotryptamine (5-CT), increased 2-h water intake by nondeprived rats (ED50 = 0.04 mumol/kg). The 5-HT1 agonists 8-hydroxy-2-(di-N-propylamino)-tetralin (8-OH-DPAT, 0.04-0.32 mumol/kg) and RU 24969 (0.16 mumol/kg) did not produce drinking. The dipsogenic effect of 5-CT (0.08 mumol/kg) was prevented by the 5-HT1/2 antagonist, methysergide (ID50 = 4 mumol/kg), but not by 16 mumol/kg of the 5-HT2 antagonist, ketanserin; the 5-HT21C antagonist, mianserin; or the 5-HT3 antagonist, MDL 72222, 5-CT also increased drinking and reduced food intake when food-deprived rats were given 2-h access to mash. Methysergide (16 mumol/kg) inhibited both actions of 5-CT but an equimolar dose of the 5-HT1/beta adrenergic antagonist, (-)-propranolol, blocked only the drinking. The 5-HT21C antagonist, ritanserin (16 mumol/kg), altered neither ingestive action of 5-CT although, by itself, ritanserin increased mash intake. The results suggest that activating a subtype of peripheral 5-HT1-like receptor stimulates drinking in rats. This receptor is unlike either the 5-HT1A or the 5-HT1C sites found in the brain. Furthermore, the dipsogenic and anorectic actions of 5-CT occur independently.
皮下注射典型的5-羟色胺1样激动剂5-羧基色胺（5-CT），可增加未禁食大鼠2小时的饮水量（半数有效量=0.04μmol/kg）。5-羟色胺1激动剂8-羟基-2-（二-N-丙基氨基）四氢萘（8-OH-DPAT，0.04 - 0.32μmol/kg）和RU 24969（0.16μmol/kg）未引起饮水增加。5-HT1/2拮抗剂美西麦角（半数抑制量=4μmol/kg）可阻止5-CT（0.08μmol/kg）的致渴作用，但16μmol/kg的5-羟色胺2拮抗剂酮色林、5-羟色胺2C拮抗剂米安色林或5-羟色胺3拮抗剂MDL 72222则不能。当给禁食大鼠2小时进食软饲料的机会时，5-CT也会增加饮水量并减少食物摄入量。美西麦角（16μmol/kg）可抑制5-CT的这两种作用，但等摩尔剂量的5-羟色胺1/β肾上腺素能拮抗剂（-）-普萘洛尔仅能阻断饮水行为。5-羟色胺2C拮抗剂利坦色林（16μmol/kg）虽本身可增加软饲料摄入量，但对5-CT的任何一种摄食作用均无影响。结果表明，激活外周5-羟色胺1样受体的一个亚型可刺激大鼠饮水。该受体与在脑中发现的5-羟色胺1A或5-羟色胺1C位点均不同。此外，5-CT的致渴和厌食作用是独立发生的。
