Lionel Cusan

Inhibitory Effect of a Luteinizing Hormone (LH)-Releasing Hormone Agonist on Rat Ovarian LH and Follicle-Stimulating Hormone Receptor Levels During Pregnancy

When injected at the daily dose of 100 microgram on days 7 through 12 of pregnancy, the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6, des-Gly-NH2(10)] LHRH ethylamide led to complete suppression of pregnancy and a 45% to 60% decrease in plasma progesterone concentration. The antifertility effect of the LHRH analog was accompanied by an early and almost complete inhibition of ovarian LH/human chorionic gonadotropin and follicle-stimulating hormone receptor levels. These data suggest that the antifertility effects of LHRH agonists are mediated by down-regulation of ovarian gonadotropin receptors and decreased luteal function.

Evidence for a role of endorphins in stress- and suckling-induced prolactin release in the rat

Injection of the opiate antagonist naloxone completely prevented the rise of serum prolactin induced by ether stress in intact male rats. Naloxone also led to a 50--95% inhibition of the marked elevation of plasma prolactin levels induced by suckling. These data suggest that endogenous opiates (endorphins) are involved in the stimulation of prolactin release induced by both stress and suckling in the rat.