Mitchell R, Sim P J, Leslie T, Johnson M S, Thomson F J
MRC Brain Metabolism Unit, Edinburgh, UK.
J Endocrinol. 1994 Feb;140(2):R15-8. doi: 10.1677/joe.0.140r015.
A MAP kinase activity assay was developed to determine whether the LHRH receptor could activate this enzyme (particularly during LHRH priming). In anterior pituitary tissue from prooestrous rats LHRH caused concentration-dependent activation of MAP kinase after 5-10 min and continued for up to 60 min of incubation. The magnitude of this response correlated with that of LHRH priming on various days of the oestrous cycle but not with the magnitude of 1st hour (unprimed) LHRH-induced LH release. The response to LHRH was mimicked by a phorbol ester but not by ionomycin and was blocked with high potency by GF 109203X but not by H7 (in a similar manner to the PKC species that mediates LHRH priming). Neither the tyrosine kinase inhibitor lavendustin A nor the protein synthesis inhibitor cycloheximide blocked LHRH-induced MAP kinase activation. The possible functional significance of MAP kinase activation in gonadotrophs is considered with respect to LHRH priming.
开发了一种丝裂原活化蛋白激酶（MAP激酶）活性测定法，以确定促性腺激素释放激素（LHRH）受体是否能激活这种酶（特别是在LHRH预刺激期间）。在动情前期大鼠的垂体前叶组织中，LHRH在孵育5 - 10分钟后引起MAP激酶浓度依赖性激活，并持续长达60分钟。这种反应的幅度与动情周期不同天数的LHRH预刺激的幅度相关，但与第1小时（未预刺激）LHRH诱导的促黄体生成素（LH）释放的幅度无关。佛波酯可模拟对LHRH的反应，而离子霉素则不能，并且GF 109203X可高效阻断该反应，而H7则不能（其方式与介导LHRH预刺激的蛋白激酶C种类相似）。酪氨酸激酶抑制剂拉文杜斯汀A和蛋白质合成抑制剂环己酰亚胺均不能阻断LHRH诱导的MAP激酶激活。关于LHRH预刺激，考虑了MAP激酶激活在促性腺细胞中的可能功能意义。
