β-内啡肽调节促肾上腺皮质激素释放因子对促黄体生成素分泌的抑制作用。

beta-Endorphin modulates the inhibitory action of corticotropin-releasing factor on luteinizing hormone secretion.

作者信息

Petraglia F, Vale W, Rivier C

机构信息

Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, La Jolla, CA 92037.

出版信息

NIDA Res Monogr. 1986;75:331-4.

PMID:2893271

Abstract

The present study investigates the possible role of endogenous opioid peptides in mediating the inhibitory effect of corticotropin-releasing factor (CRF) on circulating luteinizing hormone (LH). The central injection of an antiserum against beta-endorphin (beta-END) reversed CRF-induced LH decrease in castrated male rats, while antisera raised against DYN-A or M-Enk were inactive. beta-END-(6-31) (2 nmole, icv), a beta-END antagonist, and beta-funaltrexamine (4.8 nmole, icv), a mu 1 opiate receptor antagonist, also reversed the effect of CRF on LH. Either kappa (Mr 1456 and Mr 2266) (10 mg/kg, ip), or delta (ICI 154,129) (10 nmole, icv) opiate receptor antagonists did not significantly modify the inhibitory effect of CRF on circulating LH levels. These results suggest that central beta-END participates in the inhibitory action of CRF on LH secretion.

摘要

本研究探讨内源性阿片肽在介导促肾上腺皮质激素释放因子（CRF）对循环黄体生成素（LH）的抑制作用中可能发挥的作用。向去势雄性大鼠脑室内注射抗β-内啡肽（β-END）抗血清可逆转CRF诱导的LH降低，而针对强啡肽A（DYN-A）或甲硫氨酸脑啡肽（M-Enk）制备的抗血清则无此作用。β-END拮抗剂β-END-（6-31）（2纳摩尔，脑室内注射）和μ1阿片受体拮抗剂β-芬太尼（4.8纳摩尔，脑室内注射）也可逆转CRF对LH的作用。κ阿片受体拮抗剂（分子量1456和分子量2266）（10毫克/千克，腹腔注射）或δ阿片受体拮抗剂（ICI 154,129）（10纳摩尔，脑室内注射）均未显著改变CRF对循环LH水平的抑制作用。这些结果表明，中枢β-END参与了CRF对LH分泌的抑制作用。