Follicular phase (FOL; Days 17-19; n = 8), luteal phase (LUT; Days 7-9; n = 6), and ovariectomized (OVX; n = 5) crossbred gilts were used (Day 0 = onset of estrus). Blood samples were collected via jugular vein cannula every 15 min for 2 h the day before pituitary collection. Serum was assayed for insulin-like growth factor (IGF)-I, IGF-I binding proteins (IGFBP), LH, estradiol (E2), and progesterone (P4). Anterior pituitary cells were dispersed, cultured, and challenged on Day 4 of culture (Day 0 = day of seeding) with 10(-7) M GnRH or IGF-I (10(-11), 10(-10), 10(-9), 10(-8), or 3 x 10(-8) M) individually or in combination. Serum E2 and P4 concentrations indicated that the animals were in the appropriate stage of the estrous cycle. Mean serum LH concentrations were greater (p < 0.0004) for OVX animals compared to FOL and LUT animals. Mean serum IGF-I concentrations were lower (p < 0.05) for OVX compared to FOL and LUT animals, while serum IGFBP were not different among animals. Basal LH secretion (control) was greater (p < 0.04) in OVX than in FOL or LUT cultures. Relative to control, 10(-11) M IGF-I increased (p < 0.02) LH secretion in FOL, LUT, and OVX cultures, and this response was greater (p < 0.05) in FOL and OVX than in LUT cultures. Only the 10(-11) M IGF-I enhanced basal LH secretion in LUT cultures. In addition, 10(-10) M IGF-I increased (p < 0.05) LH secretion in OVX cultures, and 10(-10) and 10(-9) M IGF-I stimulated (p < 0.05) LH secretion in FOL cultures, whereas basal LH secretion in all groups was unaffected (p > 0.05) by 10(-8) or 3 x 10(-8) M IGF-I. The GnRH-induced LH secretion was unaltered by IGF-I treatment. Results indicate that in vitro IGF-I treatment increased basal LH secretion, with reproductive status modulating LH response to IGF-I.

No abstract

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.