The role of excitatory amino acids in pulsatile secretion of luteinizing hormone in gilts and barrows.

The relationship of excitatory amino acid (EAA) activity to LH secretion was investigated in ovariectomized crossbred prepuberal gilts (93 +/- 1 kg BW) and Yorkshire barrows (94 +/- 2 kg BW) in two experiments. In Exp. 1, eight gilts received, i.m., saline (S) or 20 mg of Ketamine (K)/kg BW, a noncompetitive EAA receptor antagonist. Within these groups, four then received 10 mg of N-methyl-DL-aspartate (NMA)/kg BW, an EAA agonist, or S i.v. Mean serum LH concentrations were similar among groups before treatment, did not change after S+S, but decreased (P < .05) by 1 h after S+NMA, 3 h after K+S, and 2 h after K+NMA. Serum cortisol concentrations did not change after S+S, but were increased (P < .05) from 30 to 90 min after S+NMA, at 120 min after K+S, and from 30 to 120 min after K+NMA. In Exp. 2, barrows received 2.5 mg of NMA/kg BW i.v. immediately after i.m. injection of S (n = 7) or 19.9 mg of K/kg BW (n = 8). Mean serum LH concentrations for the 2 h before treatment were similar among barrows, but decreased (P < .05) by 2 h after K+NMA and was not altered after S+NMA. Serum cortisol concentrations were increased at 30 min after S+NMA and from 60 to 90 min after K+NMA. We suggest that EAA both inhibit and stimulate LH secretion, with the inhibitory effects lying within the basal hypothalamus and the stimulatory effects lying within higher brain centers.