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吗啡给药后大鼠结节漏斗多巴胺神经元的延迟激活及催乳素分泌的抑制。

Delayed activation of tuberoinfundibular dopamine neurons and suppression of prolactin secretion in the rat after morphine administration.

作者信息

Gudelsky G A, Passaro E, Meltzer H Y

出版信息

J Pharmacol Exp Ther. 1986 Mar;236(3):641-5.

PMID:3950867
Abstract

The effect of morphine administration on the subsequent stimulation of prolactin (PRL) secretion and the release of dopamine from tuberoinfundibular neurons was examined in this study. The administration of morphine (15 mg/kg s.c.) resulted 4 hr later in suppressed serum PRL concentrations. In addition, the increase in serum PRL concentrations induced by restraint stress was attenuated greatly in rats treated 4 hr earlier with morphine. The morphine-induced attenuation of the PRL response to restraint stress was time-dependent and dose-related. The suppressive effect of morphine on PRL secretion was observed 3 to 6 hr after its administration and at doses of 10 to 20 mg/kg. A single injection of morphine also resulted 4 hr later in an attenuation of the PRL response to a second injection of morphine (7.5 mg/kg); however, the increase in serum PRL concentration produced by alpha-methyltyrosine (250 mg/kg) was unaltered by prior morphine administration. The suppressive effect of morphine on PRL secretion was not observed in rats treated with the opiate antagonist naloxone (2.5 mg/kg). Associated with the delayed suppressive effect of morphine on serum PRL concentrations was a delayed increase in the concentration of dopamine in hypophysial portal plasma and an increase in the turnover of dopamine in the median eminence. The morphine-induced stimulation of the release of dopamine into hypophyseal portal blood was attenuated significantly in animals treated with naltrexone (1 mg/kg). It is concluded that morphine exerts a biphasic effect on both the secretion of PRL and the release of dopamine from tuberoinfundibular neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究检测了吗啡给药对随后催乳素(PRL)分泌刺激以及来自结节漏斗神经元的多巴胺释放的影响。皮下注射吗啡(15毫克/千克)4小时后导致血清PRL浓度受到抑制。此外,在4小时前用吗啡处理的大鼠中,束缚应激诱导的血清PRL浓度升高被大大减弱。吗啡诱导的对束缚应激的PRL反应减弱具有时间依赖性且与剂量相关。在给药后3至6小时以及剂量为10至20毫克/千克时观察到吗啡对PRL分泌的抑制作用。单次注射吗啡4小时后也导致对第二次注射吗啡(7.5毫克/千克)的PRL反应减弱;然而,α-甲基酪氨酸(250毫克/千克)产生的血清PRL浓度升高并未因先前给予吗啡而改变。在用阿片拮抗剂纳洛酮(2.5毫克/千克)处理的大鼠中未观察到吗啡对PRL分泌的抑制作用。与吗啡对血清PRL浓度的延迟抑制作用相关的是垂体门脉血浆中多巴胺浓度的延迟升高以及正中隆起中多巴胺周转率的增加。在用纳曲酮(1毫克/千克)处理的动物中,吗啡诱导的多巴胺释放到垂体门脉血中的刺激作用显著减弱。结论是,吗啡对PRL分泌以及来自结节漏斗神经元的多巴胺释放均产生双相作用。(摘要截短至250字)

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