Murakami Y, Kato Y, Shimatsu A, Koshiyama H, Hattori N, Yanaihara N, Imura H
Department of Medicine, Kyoto University Faculty of Medicine, Japan.
Endocrinology. 1989 Mar;124(3):1224-9. doi: 10.1210/endo-124-3-1224.
The mechanisms by which central or systemic administration of galanin stimulates GH secretion were investigated in either conscious or urethane-anesthetized male rats. Intracerebroventricular injection of synthetic porcine galanin, a 29-amino acid gut-brain peptide (0.12, 0.6, and 3 nmol/rat), resulted in a dose-related increase in plasma GH. The plasma GH level was increased by an N-terminal galanin fragment [galanin-(1-19)], but not by C-terminal fragments [galanin-(2-29) and -(21-29)]. Intravenous injection or infusion of galanin (0.6 and 3 nmol/100 g BW) also raised plasma GH. The plasma GH increase induced by galanin was inhibited by pretreatment with rabbit antiserum specific for rat GRF. Pretreatment with yohimbine or phenoxybenzamine, alpha-adrenergic blockers, or picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, blunted the plasma GH increase induced by intracerebroventricular injection of galanin. On the other hand, the plasma GH increase induced by iv injection of galanin was suppressed by picrotoxin, but not by phenoxybenzamine. These findings suggest that 1) both central and systemic administration of galanin stimulate GH secretion in the rat; 2) the N-terminal structure of galanin is required to stimulate GH secretion; 3) the stimulating effect of galanin is mediated, at least in part, by hypothalamic GRF; and 4) central alpha-adrenergic and GABAergic mechanisms may be involved in GH release induced by central administration of galanin, whereas systemic injection of galanin stimulates GH release predominantly through GABAergic mechanisms in the rat.
在清醒或氨基甲酸乙酯麻醉的雄性大鼠中，研究了甘丙肽中枢或全身给药刺激生长激素（GH）分泌的机制。向大鼠脑室内注射合成猪甘丙肽（一种含29个氨基酸的肠脑肽，剂量为0.12、0.6和3 nmol/只大鼠），可导致血浆GH呈剂量相关增加。N端甘丙肽片段[甘丙肽-(1-19)]可使血浆GH水平升高，但C端片段[甘丙肽-(2-29)和-(21-29)]则无此作用。静脉注射或输注甘丙肽（0.6和3 nmol/100 g体重）也可使血浆GH升高。甘丙肽诱导的血浆GH升高可被用针对大鼠生长激素释放因子（GRF）的兔抗血清预处理所抑制。用育亨宾或酚苄明（α-肾上腺素能阻滞剂）或苦味毒（一种γ-氨基丁酸（GABA）拮抗剂）预处理，可减弱脑室内注射甘丙肽诱导的血浆GH升高。另一方面，静脉注射甘丙肽诱导的血浆GH升高可被苦味毒抑制，但不能被酚苄明抑制。这些发现表明：1）甘丙肽中枢和全身给药均可刺激大鼠GH分泌；2）甘丙肽刺激GH分泌需要其N端结构；3）甘丙肽的刺激作用至少部分是由下丘脑GRF介导的；4）中枢α-肾上腺素能和GABA能机制可能参与了中枢给予甘丙肽诱导的GH释放，而全身注射甘丙肽在大鼠中主要通过GABA能机制刺激GH释放。
