Moguilevsky J A, Carbone S, Szwarcfarb B, Rondina D, Scacchi P
Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, Paraguay, Argentina.
J Steroid Biochem Mol Biol. 1995 Jun;53(1-6):337-41. doi: 10.1016/0960-0760(95)00079-f.
The present results indicate that during sexual maturation the APOA-MBH from rats of 30 days of age released significantly higher quantities of GnRH than the tissue from 16-day-old rats (P < 0.01). The addition of NMDA, an agonist of the excitatory amino acids system (EAAs), to the medium after 30 min of incubation significantly increased (P < 0.01) the GnRH release in normal rats of both ages and this increase was significantly (P < 0.01) higher in 30-day-old rats (to 661%) than in rats of 16 days of age (to 273%). The administration of estrogen-progesterone (EP) to rats of 16 days of age did not modify the GnRH release response to NMDA. On the contrary, at 30 days of age EP administration significantly potentiated the GnRH release response to NMDA since while in the control group NMDA increased the GnRH release to 630%, in the EP-pretreated group this was to around 4700% (P < 0.01). EP pretreatment of prepubertal rats decreases the hypothalamic release of aspartate and glutamate, the excitatory amino acids involved in NMDA neurotransmission and glycine but increases EAAs release in peripubertal rats. On the basis of these results it is proposed that the increase in EAAs release by the hypothalamus is directly connected with the onset of puberty and that the maturation of the positive feedback effect of ovarian hormones on gonadotropin secretion is related to the maturation of the capacity of EP to increase hypothalamic EAAs. Before this maturational event EP inhibits EAAs release as well as gonadotropin release (prepubertal rats). NMDA receptor stimulation leads to a positive mechanism which increases the release of Asp and Glu from APOA-MBH both in prepubertal and peripubertal rats, but EP potentiates this mechanism only in peripubertal rats. This could be an additional neuroendocrine mechanism involved in the increase of gonadotropin during sexual maturation which induces the onset of puberty and the preovulatory discharge of these pituitary hormones.
目前的结果表明,在性成熟过程中,30日龄大鼠的弓状核-内侧基底下丘脑(APOA-MBH)释放的促性腺激素释放激素(GnRH)量显著高于16日龄大鼠的组织(P < 0.01)。孵育30分钟后,向培养基中添加兴奋性氨基酸系统(EAAs)的激动剂N-甲基-D-天冬氨酸(NMDA),显著增加了(P < 0.01)两个年龄组正常大鼠的GnRH释放,且30日龄大鼠的这种增加幅度(达到661%)显著高于(P < 0.01)16日龄大鼠(达到273%)。对16日龄大鼠给予雌激素-孕激素(EP)并未改变其对NMDA的GnRH释放反应。相反,在30日龄时,给予EP显著增强了对NMDA的GnRH释放反应,因为在对照组中NMDA使GnRH释放增加到630%,而在EP预处理组中这一比例约为4700%(P < 0.01)。青春期前大鼠经EP预处理后,下丘脑天冬氨酸和谷氨酸(参与NMDA神经传递的兴奋性氨基酸)以及甘氨酸的释放减少,但青春期大鼠的EAAs释放增加。基于这些结果,有人提出下丘脑EAAs释放的增加与青春期的开始直接相关,卵巢激素对促性腺激素分泌的正反馈作用的成熟与EP增加下丘脑EAAs的能力的成熟有关。在这一成熟事件之前,EP抑制EAAs释放以及促性腺激素释放(青春期前大鼠)。NMDA受体刺激导致一种正向机制,在青春期前和青春期大鼠中均增加弓状核-内侧基底下丘脑的天冬氨酸(Asp)和谷氨酸(Glu)释放,但EP仅在青春期大鼠中增强这种机制。这可能是性成熟过程中促性腺激素增加所涉及的另一种神经内分泌机制,它诱导青春期的开始以及这些垂体激素的排卵前释放。