Rivier C, Rivest S
Clayton Foundation Laboratories for Peptide Biology, Salk Institute, La Jolla, California 92037.
Biol Reprod. 1991 Oct;45(4):523-32. doi: 10.1095/biolreprod45.4.523.
This article reviews the mechanisms believed to mediate stress-induced inhibition of reproductive functions and the anatomical sites at which these effects take place. Particular emphasis is placed on the potential modulating role of hormones or neurotransmitters released during stress. At the level of the gonads, adrenal corticoids, pro-opiomelanocortin (POMC)-like peptides, and corticotropin-releasing factor (CRF) are reported to interfere with the stimulatory action of gonadotropins on sex steroid-producing cells. Increased circulating corticosteroid levels may also decrease pituitary responsiveness to GnRH. There is, however, increasing evidence that these mechanisms are primarily involved in mediating the effects of prolonged stress, but not those of an acute stimulus. In contrast, a variety of hormones or neurotransmitters, including CRF, POMC peptides, and biogenic amines act within the brain to mediate the inhibitory influence of both acute and prolonged stresses on reproductive function.
本文综述了被认为介导应激诱导的生殖功能抑制的机制以及这些效应发生的解剖部位。特别强调了应激期间释放的激素或神经递质的潜在调节作用。在性腺水平，据报道肾上腺皮质激素、促阿片黑素皮质素（POMC）样肽和促肾上腺皮质激素释放因子（CRF）会干扰促性腺激素对产生性类固醇细胞的刺激作用。循环中皮质类固醇水平的升高也可能降低垂体对促性腺激素释放激素（GnRH）的反应性。然而，越来越多的证据表明，这些机制主要参与介导长期应激的效应，而非急性刺激的效应。相比之下，包括CRF、POMC肽和生物胺在内的多种激素或神经递质在脑内发挥作用，介导急性和长期应激对生殖功能的抑制影响。
