Pulsatile luteinizing hormone responses to intermittent iv-methyl-d, l-aspartate administration in hamsters exposed to long- and short-day photoperiods

John M. Meredith, Fred W. Torek, Jon E. Levine*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Hamsters exposed to short-day photoperiods (6-h light, 18-h darkness) develop a reversible inhibition of the reproductive axis which includes decreased LH pulse frequency, decreased FSH and testosterone levels, testicular regression, and presumably, decreased luteinizing hormone-releasing hormone (LHRH) release. The decrease in LHRH release could reflect a decrease in the ability of LHRH neurons to release the decapep-tide in response to intermittent neuronal excitation. To analyze this possibility, the LHRH secretagogue, N-methyl-D-aspartate (NMA) was used to estimate relative releasability of endogenous LHRH pulses in hamsters exposed to long- and short-day photoperiods. Long-day (LD) or short-day (SD) hamsters were fitted with indwelling atrial catheters 2 days before experimentation. During 5-h sampling sessions (1300-1800 h), blood was withdrawn at 10-min intervals. In initial experiments, a NMA dose-response analysis revealed that 10 and 20 mg/kg NMA but not 2.5 and 5 mg/kg NMA, produced significant, dose-related LH responses in LD hamsters. Treatments with LHRH antagonist 4 h prior to NMA treatment completely blocked LH responses. The 10 mg/kg NMA dose was then used to directly compare LHRH responsiveness in LD and SD hamsters. NMA injections were administered to groups of LD and SD hamsters after hours 1, 2, 3, and 4 of sampling. In LD hamsters, LH responses to the first NMA pulse (2.65 ± 0.09) were followed by diminishing responses to the second, third, and fourth NMA pulses (1.22 ± 0.50, 1.22 ± 0.43, and 1.15 ± 0.42). By contrast, initial LH responses in SD hamsters (1.61 ± 0.31) were followed by even more robust LH responses to the second, third, and fourth NMA challenges (2.89 ± 0.34, 3.08 ± 0.59, 2.65 ± 0.32). Although LH responses to the first NMA pulse were slightly less in SD vs. LD animals, responses to all subsequent injections were actually greater in SD hamsters vs. their LD counterparts. Injections of 20 ng/kg LHRH in SD hamsters produced LH responses similar to those evoked by NMA. The same LHRH dose also produced continued, robust LH responses in LD hamsters, indicating that decrements in response to NMA were not due to diminished pituitary responsiveness. These results suggest that 1) the stimulatory actions of NMA are mediated by LHRH, 2) exposure to short days does not decrease the responsiveness of LHRH neurons to NMA, and 3) successive NMA challenges produce diminishing LH responses in LD hamsters, but not in SD hamsters. It is hypothesized that SD-induced inhibition of the reproductive axis is not mediated by the ability of LHRH neurons to secrete LHRH. Rather, the inhibition may be imposed upstream from the secretory process, perhaps at the level of the LHRH pulse generator. Response decrements to NMA in LD hamsters may therefore reflect diminishment of the LHRH releasable pool, possibly as a secondary consequence of increased LHRH pulse generator activity.

Original languageEnglish (US)
Pages (from-to)1714-1720
Number of pages7
JournalEndocrinology
Volume129
Issue number4
DOIs
StatePublished - Oct 1991

ASJC Scopus subject areas

  • Endocrinology

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