Koshiyama H, Shimatsu A, Kato Y, Assadian H, Hattori N, Ishikawa Y, Tanoh T, Yanaihara N, Imura H
Department of Internal Medicine, Kyoto University Faculty of Medicine, Japan.
Brain Res. 1990 Jan 22;507(2):321-4. doi: 10.1016/0006-8993(90)90290-r.
The mechanism by which galanin (GAL) stimulates prolactin (PRL) secretion was investigated in urethane-anesthetized male rats. The PRL release induced by intracerebroventricular (i.c.v.) injection of porcine GAL (pGAL) was similar to that induced by rat GAL. The PRL release induced by pGAL was partially blocked by alpha-adrenergic antagonists, phentolamine (1 microgram/rat, i.c.v.; 29.1 +/- 4.5 ng/ml vs control 66.9 +/- 10.2 ng/ml, P less than 0.01) and tolazoline (1 microgram/rat, i.c.v.; 25.9 +/- 4.4 ng/ml vs control 59.6 +/- 10.9 ng/ml, P less than 0.05). Neither propranolol (1 microgram/rat, i.c.v.), a beta-adrenergic antagonist, nor prazosin (1 microgram/rat, i.c.v.), an alpha 1-adrenergic antagonist, inhibited pGAL-induced PRL release. Naloxone (125 micrograms/100 g body wt., i.v. 30 min before), an opiate antagonist, also inhibited pGAL-induced PRL release (25.9 +/- 4.0 ng/ml vs 59.1 +/- 7.2 ng/ml, P less than 0.01). Combined treatment with naloxone and phentolamine caused greater inhibition of pGAL-induced PRL release than did phentolamine alone (10.3 +/- 1.5 ng/ml vs 23.2 +/- 4.7 ng/ml, P less than 0.05), but the inhibition was similar to that induced by naloxone alone. These findings suggest that alpha 2-adrenergic and opioidergic mechanisms are involved in PRL release induced by GAL.
在氨基甲酸乙酯麻醉的雄性大鼠中研究了甘丙肽（GAL）刺激催乳素（PRL）分泌的机制。脑室内（i.c.v.）注射猪甘丙肽（pGAL）诱导的PRL释放与大鼠甘丙肽诱导的相似。pGAL诱导的PRL释放被α-肾上腺素能拮抗剂酚妥拉明（1微克/大鼠，i.c.v.；29.1±4.5纳克/毫升，对照组为66.9±10.2纳克/毫升，P<0.01）和妥拉唑啉（1微克/大鼠，i.c.v.；25.9±4.4纳克/毫升，对照组为59.6±10.9纳克/毫升，P<0.05）部分阻断。β-肾上腺素能拮抗剂普萘洛尔（1微克/大鼠，i.c.v.）和α1-肾上腺素能拮抗剂哌唑嗪（1微克/大鼠，i.c.v.）均未抑制pGAL诱导的PRL释放。阿片拮抗剂纳洛酮（125微克/100克体重，静脉注射，提前30分钟）也抑制了pGAL诱导的PRL释放（25.9±4.0纳克/毫升，对照组为59.1±7.2纳克/毫升，P<0.01）。纳洛酮和酚妥拉明联合治疗比单独使用酚妥拉明对pGAL诱导的PRL释放的抑制作用更强（10.3±1.5纳克/毫升，对照组为23.2±4.7纳克/毫升，P<0.05），但抑制作用与单独使用纳洛酮相似。这些发现表明α2-肾上腺素能和阿片样物质机制参与了GAL诱导的PRL释放。
