Carbone S, Szwarcfarb B, Rondina D, Feleder C, Moguilevsky J A
Departamento de Fisiologia, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Brain Res. 1996 Jan 29;707(2):139-45. doi: 10.1016/0006-8993(95)01216-8.
The present experiments describe the effect of NMDA and kainate agonists of the NMDA and non-NMDA subtype of receptors respectively of the excitatory amino acids (EAAs) system in prepubertal (16 days of age) and peripubertal (30-day-old rats) male rats on the in vitro hypothalamic release of GnRH, and on the in vivo LH and FSH levels as well as the effect of testosterone on these effects. The addition of NMDA or kainate to the medium containing APOA-MBH areas significantly increased (P < 0.01) the GnRH release as compared with the respective controls. The increase in GnRH release observed with kainate was significantly higher (P < 0.01) than those observed with NMDA. NMDA administration increased significantly (P < 0.01) serum LH levels at both ages of sexual maturation while no effect was observed by kainate administration. MK 801, an antagonist of NMDA neurotransmission, and testosterone abolished the LH release response to NMDA. Contrary to that observed on LH, while NMDA did not modify serum FSH concentrations a significant increase (P < 0.01) was observed with kainate administration in prepubertal and peripubertal rats on this pituitary hormone, and CNQX, an antagonist of non-NMDA neurotransmission, and testosterone administrations blocked this FSH release effect of kainate. The NMDA and kainate release effect on LH and FSH respectively was significantly higher in prepubertal than in peripubertal rats. At both ages NMDA released more LH than kainate FSH. In conclusion, our experiments demonstrated that both subtypes of glutamate receptors NMDA and non-NMDA subtypes of EAAs increased GnRH release by APOA-MBH in vitro during sexual maturation. Nevertheless, while NMDA administration only increased serum LH levels, kainate showed only an effect on increasing FSH concentrations. These differential effects of NMDA and non-NMDA subtypes of EAA receptors on LH and FSH could probably explain some aspects of the differential modifications of LH and FSH observed in different physiological circumstances.
本实验描述了兴奋性氨基酸(EAA)系统中NMDA和非NMDA亚型受体的激动剂NMDA和海人酸,分别对青春期前(16日龄)和青春期前后(30日龄大鼠)雄性大鼠下丘脑体外GnRH释放、体内LH和FSH水平的影响,以及睾酮对这些影响的作用。与各自的对照组相比,在含有APOA - MBH区域的培养基中添加NMDA或海人酸显著增加了(P < 0.01)GnRH的释放。海人酸引起的GnRH释放增加显著高于(P < 0.01)NMDA引起的增加。在两个性成熟年龄阶段,NMDA给药均显著增加了(P < 0.01)血清LH水平,而海人酸给药未观察到影响。NMDA神经传递拮抗剂MK 801和睾酮消除了对NMDA的LH释放反应。与对LH的观察结果相反,虽然NMDA未改变血清FSH浓度,但在青春期前和青春期前后的大鼠中,海人酸给药对这种垂体激素有显著增加(P < 0.01),非NMDA神经传递拮抗剂CNQX和睾酮给药阻断了海人酸的这种FSH释放作用。青春期前大鼠中,NMDA和海人酸对LH和FSH的释放作用分别显著高于青春期前后的大鼠。在两个年龄阶段,NMDA释放的LH比海人酸释放的FSH更多。总之,我们的实验表明,在性成熟期间,EAA的谷氨酸受体的NMDA和非NMDA两种亚型在体外均增加了APOA - MBH的GnRH释放。然而,虽然NMDA给药仅增加血清LH水平,但海人酸仅对增加FSH浓度有作用。EAA受体的NMDA和非NMDA亚型对LH和FSH的这些不同作用可能解释了在不同生理情况下观察到的LH和FSH的不同变化的某些方面。