Smith W A, Conn P M
Endocrinology. 1983 Jan;112(1):408-10. doi: 10.1210/endo-112-1-408.
In the present work we describe homologous desensitization of gonadotropin release from pituitary cells in response to short-term exposure to GnRH. Like the release process itself, desensitization requires receptor occupancy by an agonist. In contrast, however, inhibition of LH release by chelation of extracellular calcium or blockade of the calcium ion channel does not inhibit desensitization. Further, stimulation of gonadotropin release by ionophore A23187 (which mobilizes calcium without GnRH receptor occupancy) does not lead to desensitization. These findings indicate that the decrease in pituitary sensitivity to GnRH due to an initial exposure to the peptide can be uncoupled from LH release. The data provide the first evidence of a calcium-independent biological effect of the releasing hormone in cultured pituitary cells.
在本研究中，我们描述了垂体细胞中促性腺激素释放对短期暴露于促性腺激素释放激素（GnRH）的同源脱敏现象。与释放过程本身一样，脱敏需要激动剂占据受体。然而，与之相反的是，通过螯合细胞外钙或阻断钙离子通道来抑制促黄体生成素（LH）释放并不会抑制脱敏。此外，离子载体A23187（其在不占据GnRH受体的情况下动员钙）刺激促性腺激素释放并不会导致脱敏。这些发现表明，由于最初暴露于该肽而导致的垂体对GnRH敏感性降低可与LH释放脱钩。这些数据首次证明了释放激素在培养的垂体细胞中存在不依赖钙的生物学效应。
