The role of N-methyl-D-aspartate (NMDA) receptor activation in the central regulation of luteinizing hormone (LH) and growth hormone (GH) was tested by administering a bolus intravenous dose of N-methyl-D,L-aspartic acid (NMA), a NMDA receptor agonist, to 24-week-old intact (n=5), estradiol-treated intact (n=3) and castrated (n=3) Holstein bull calves. The calves were bled for 12h pre- and 100 min post-NMA injection (1.75 mg-/kgBW) periods at 10 min intervals. Concentrations of LH and GH in plasma were measured by specific RIA. Prior to administration of NMA, the average concentration of LH, but not GH, differed significantly among the 3 groups. As expected, administration of estradiol prevented the normal ontogeny of pulsatile LH secretion, while castration resulted in an increased frequency of LH discharges. Injection of NMA resulted in an acute (P<0.001) release of LH in 3 of 5 intact and 3 of 3 estradiol-treated intact calves with the peak response being observed at 20 min (3.18 +/- 1.3 and 5.58 +/- 1.3 ng/ml, respectively) following the challenge. Treatment with NMA did not alter the release of LH in castrate calves. Concentrations of GH in plasma increased (P<0.001) within 20 to 30 min after administration of NMA in intact, estradiol-treated intact and castrate calves with a similar response being observed in each group. Based on these findings, we suggest an involvement of glutamatergic neurotransmission in the hypothalamic or supra-hypothalamic control of LH and GH secretion, and that the excitatory effects of NMDA receptor activation on LH release are overtly influenced by gonadal steroids in bull calves.