The glutamate receptor agonist, N-methyl-D-aspartate (NMDA), can profoundly stimulate luteinizing hormone (LH) secretion.
The aim of this study was to examine the possibility that adrenergic inputs to the LHRH neurons play a key role in mediating the EAA-induced release of LHRH/LH in the gonadal-intact female rhesus macaque. On three consecutive days, mature rhesus females were pre-treated intravenously either with physiological saline, prazosin (an `1-adrenergic receptor antagonist), or with idazoxan (an `2-adrenergic receptor antagonist); either 10 or 40 min after each pre-treatment, NMDA (10 mg/kg body weight) was administered intravenously and for the next hour serial 10-min blood samples were collected through indwelling jugular vein catheters. The plasma was subsequently assayed for LH using a mouse Leydig cell bioassay. As expected, from previous observations, the animals showed little or no increase in plasma LH in response to NMDA during the follicular phase of the menstrual cycle but showed a rapid (i.e., <10 minutes) and highly significant increase during the luteal phase. On the other hand, this stimulatory response to NMDA could neither be blocked nor attenuated by pre-treatment with prazosin, using a dose that markedly inhibited pulsatile LH release in ovariectomized macaques (1 - 5 mg/kg body weight); idazoxan also failed to suppress the LH response to NMDA. Taken together, therefore, these data do not support the view that adrenergic neurons play a key role in mediating EAA-induced release of LHRH/LH secretion and suggest that the stimulatory action of EAAs is likely either to involve some other inter-neuronal pathways or to be exerted directly at the level of the LHRH neurons themselves. (Findings from this study were presented in 1995 at the Annual Meeting of the Society for the Study of Reproduction, held in Davis, CA).
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