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Involvement of N-methyl-D-aspartate receptor using excitatory amino acid neurotransmitters in control of pulsatile secretion of LH during sexual development in Holstein bull calves

The neuroendocrine mechanisms underlying the development of pulsatile release of LH in bull calves are poorly understood. The hypothesis that endogenous excitatory amino acids, working through N-methyl-D-aspartate (NMDA) receptors, are involved in the generation of pulsatile LH release during sexual maturation of bull calves was tested. Holstein bull calves were administered i.v. 0.001, 0.01 and 0.1 mg kg^–1 body mass of MK-801, a specific noncompetitive NMDA receptor antagonist, on alternate days at 1, 12 and 24 weeks of age (n = 6 per dose), using a replicated 3x3 latin square design. Blood samples were obtained from jugular catheters at intervals of 10 min for 2 h before and 2 h after MK-801 treatment at 1 week and for periods of 4 h before and after MK-801 administration at 12 and 24 weeks of age. Plasma concentrations of LH were measured by a specific radioimmunoassay and pulsatile LH secretion was analysed using the Pulsar algorithm. Basal LH secretion at 1 week of age was low but was increased by 12 weeks (0.38 ± 0.01 versus 1.38 ± 0.11 ng ml^–1; P < 0.001) with the establishment of frequent high amplitude pulses. Mean LH concentrations and pulse amplitude, but not frequency, were lower at 24 than at 12 weeks of age (0.88 ±0.08 versus 1.38 ± 0.11 ng ml^–1: P < 0.001, 1.74 ± 0.14 versus 2.82 ± 0.36 ng ml^–1: P < 0.01, and 1.70 ± 0.30 versus 1.70 ± 0.41 in 4 h: P > 0.05, respectively). Administration of MK-801 did not affect LH secretion in 1- and 12-week-old calves. In contrast, the antagonist at the highest dose tested caused a significant decrease in mean LH concentrations (0.30 ± 0.01 versus 0.70 ±0.10 ng ml^–1; P < 0.05), which was associated with a reduction in the number of LH pulses (0.70 ± 0.30 versus 1.50 ± 0.30 in 4 h; P < 0.01) and pulse amplitude (0.54 ± 0.04 versus 1.72 ± 0.20 ng ml^–1; P < 0.001), in 24-week-old calves. These data suggest that the initiation of pulsatile secretion of LH during the juvenile phase in bull calves is not mediated by the endogenous excitatory amino acids operating through NMDA receptors. However, maintenance of the pulsatile secretory pattern of LH in prepubertal bull calves, which is required for continued testicular maturation, does involve an NMDA-receptor-mediated neuroexcitatory drive to GnRH-releasing neurones.

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