Summary. It has been suggested that changes in endogenous glutamatergic stimulation of secretion of luteinizing hormone (LH) induced by photoperiod play a role in regulating seasonal cycles of reproductive activity. The aim of this study was to test the hypothesis that the glutamatergic control of the secretion of LH in the male Syrian hamster is sensitive to photoperiod, by determining whether the glutamate agonist Nmethyl-d-aspartate (NMDA) could stimulate LH secretion in this species and, if so, to determine whether the response varied among animals exposed to different daylengths. In the first experiment, adult male hamsters were housed in either short days (8 h light: 16 h dark) for 6 weeks to induce testicular regression, or long days (16 h light:8 h dark) to maintain testicular function, and the effects of systemic administration of NMDA on serum LH concentrations were determined. In the short-day hamsters, all s.c. doses of NMDA (25–75 mg kg−1 body weight) produced a robust rise in serum LH concentrations within 15 min. In the long-day hamsters, basal LH concentrations were higher than in short-day hamsters, but only the highest dose of NMDA produced a significant increase in LH concentrations, and the magnitude of this increment was less than those observed in short days. In hamsters in long days, the low doses of NMDA that did not significantly alter LH concentrations nevertheless significantly suppressed serum prolactin concentrations, demonstrating the efficacy of the drug. In hamsters in short days, serum prolactin concentrations were at the limit of detection of the assay, so no inhibitory effect of NMDA on prolactin secretion could be determined on this photoperiod. In the second experiment, the effects of a fixed dose of NMDA (50 mg kg−1 body weight) was tested at intervals in hamsters exposed to short days for a prolonged period such that their testes initially regressed, but then became scotorefractory and testicular recrudescence occurred. After 6 and 12 weeks in short days, NMDA stimulated LH secretion. However, after 24 weeks in short days when testicular recrudescence was complete, the response to NMDA was lost. A third experiment determined whether the reduced response to NMDA in hamsters on long days relative to those in short days might result from higher concentrations of circulating testosterone. Hamsters in long days were castrated to remove the influence of gonadal feedback, and the response to NMDA tested 3 weeks later when endogenous LH concentrations had risen to levels characteristic of the chronically castrated condition. NMDA significantly reduced serum LH in castrated hamsters. Thus, the increased LH response to NMDA in hamsters in short days is unlikely to reflect the very low serum testosterone concentrations at this time. A preliminary experiment was conducted with the glutamate antagonist MK801 to investigate whether endogenous glutamatergic mechanisms support LH secretion in hamsters in long days. Systemic treatment with MK801 (0·6 mg kg−1 body weight, i.p.) did not significantly alter LH concentrations at 30 or 60 min after injection, though this dose did increase LH secretion in castrate hamsters as might be expected in view of the paradoxical inhibitory action of NMDA in castrates. Although this acute experimental paradigm did not provide direct evidence for endogenous glutamatergic control of LH in sexually active hamsters, the increased sensitivity and responsiveness to the agonist NMDA in hamsters in short days is consistent with the view that endogenous glutamatergic stimulation is decreased in this photoperiod, and that this decreased activity contributes to the regression of the reproductive axis.
Keywords: photoperiod; NMDA; LH; prolactin; hamster; season
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