Differential effects of the N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors of the excitatory amino acids system on LH and FSH secretion. Its effects on the hypothalamic luteinizing hormone releasing hormone during maturation in male rats

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.