Morley J E, Levine A S, Murray S S, Kneip J, Grace M
Am J Physiol. 1982 Jul;243(1):R159-63. doi: 10.1152/ajpregu.1982.243.1.R159.
By use of the model of stress-induced (mild tail pinch) eating we have examined the interrelationships of peptides and monoamines responsible for regulating this behavior. We have shown that the synthetic opiate analog, D-Ala2-Met-enkephalinamide (1 microgram), when administered intracerebroventricularly (icv) reverses the suppressive effects of the serotonin agonist, quipazine (40 micrograms icv), the beta-agonist, isoproterenol (40 micrograms icv), and the alpha-antagonist, phentolamine (150 micrograms icv), and partially reversed the effects of atropine (2.5 mg/kg sc) and the dopamine antagonist haloperidol (0.5 mg/kg sc). The opiate antagonist naloxone (10 mg/kg sc) suppressed tail-pinch-induced eating, and this effect could not be reversed by the GABA-agonist muscimol (500 ng icv) nor norepinephrine (20 micrograms icv). The putative satiety hormones cholecystokinin-octapeptide (5 micrograms/kg sc) and bombesin (5 micrograms/kg sc) suppressed stress-induced eating. The suppressive effect of these substances was reversed by a number of known appetite stimulants viz., D-Ala2-Met-enkephalinamide, diazepam, muscimol, and propanolol. Norepinephrine reversed the suppressive effect of bombesin but not that of cholecystokinin. Based on these results we present a hypothetical model to partially explain the peptidergic-monoamine regulation of stress-induced eating.
通过使用应激诱导（轻度夹尾）进食模型，我们研究了负责调节这种行为的肽类和单胺类之间的相互关系。我们已经表明，合成阿片类类似物D - Ala2 - Met - 脑啡肽酰胺（1微克），当脑室内（icv）给药时，可逆转5 - 羟色胺激动剂喹哌嗪（icv 40微克）、β激动剂异丙肾上腺素（icv 40微克）和α拮抗剂酚妥拉明（icv 150微克）的抑制作用，并部分逆转阿托品（2.5毫克/千克皮下注射）和多巴胺拮抗剂氟哌啶醇（0.5毫克/千克皮下注射）的作用。阿片拮抗剂纳洛酮（10毫克/千克皮下注射）抑制夹尾诱导的进食，且这种作用不能被GABA激动剂蝇蕈醇（icv 500纳克）或去甲肾上腺素（icv 20微克）逆转。假定的饱腹感激素胆囊收缩素八肽（5微克/千克皮下注射）和蛙皮素（5微克/千克皮下注射）抑制应激诱导的进食。这些物质的抑制作用可被多种已知的食欲刺激剂逆转，即D - Ala2 - Met - 脑啡肽酰胺、地西泮、蝇蕈醇和普萘洛尔。去甲肾上腺素逆转了蛙皮素的抑制作用，但未逆转胆囊收缩素的抑制作用。基于这些结果，我们提出了一个假设模型来部分解释应激诱导进食的肽能 - 单胺调节。
