Petraglia F, Vale W, Rivier C
Clayton Foundation Laboratories for Peptide Biology, Salk Institute for Biological Studies, La Jolla, CA 92037.
NIDA Res Monogr. 1986;75:331-4.
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.
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。
