This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MEREDITH, J. M. Articles by LEVINE, J. E. Search for Related Content PubMed PubMed Citation Articles by MEREDITH, J. M. Articles by LEVINE, J. E.

Pulsatile Luteinizing Hormone Responses to Intermittent iV-Methyl-D,L- Aspartate Administration in Hamsters Exposed to Long- and Short-Day Photoperiods^*

Department of Neurobiology and Physiology, Northwestern University Euamston, Illinois 60208

Address all correspondence and requests for reprints to: Jon E. Levine, Ph.D., Department of Neurobiology and Physiology, 2153 Sheridan Road, Evanston, Illinois 60208.

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-re leasing hormone (LHRH) release. The decrease in LHRH release could reflect a decrease in the ability of LHRH neurons to release the decapeptide in response to intermittent neuronal excitation. To analyze this possibility, the LHRH secretagogue, AT-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 During 5-h sampling sessions (1300–1800 h), blood was withdrawn at 10-min intervals.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 doseresponse 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 us. 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. (Endocrinology 129: 1714–1720,1991)

Footnotes

^* This research was supported by NIH R01 HD-20677 (J.E.L.), NIH ROl HD-09885 (F.W.T.), NIH P01 HD-21921 (J.E.L., F.W.T.), NIH K04-HD00879 (R.C.D.A. to J.E.L,),

Received July 5, 1991.

This article has been cited by other articles:

				M. Avigdor, S. D. Sullivan, and P. D. Heideman Response to selection for photoperiod responsiveness on the density and location of mature GnRH-releasing neurons Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2005; 288(5): R1226 - R1236. [Abstract] [Full Text] [PDF]

				S. Anand, S. Losee-Olson, F. W. Turek, and T. H. Horton Differential Regulation of Luteinizing Hormone and Follicle-Stimulating Hormone in Male Siberian Hamsters by Exposure to Females and Photoperiod Endocrinology, June 1, 2002; 143(6): 2178 - 2188. [Abstract] [Full Text] [PDF]

				S. L. Meddle, D. L. Maney, and J. C. Wingfield Effects of N-Methyl-D-Aspartate on Luteinizing Hormone Release and Fos-Like Immunoreactivity in the Male White-Crowned Sparrow (Zonotrichia leucophrys gambelii) Endocrinology, December 1, 1999; 140(12): 5922 - 5928. [Abstract] [Full Text]

				T. Porkka-Heiskanen, N. Khoshaba, K. Scarbrough, J. H. Urban, M. H. Vitaterna, J. E. Levine, F. W. Turek, and T. H. Horton Rapid photoperiod-induced increase in detectable GnRH mRNA-containing cells in Siberian hamster Am J Physiol Regulatory Integrative Comp Physiol, December 1, 1997; 273(6): R2032 - R2039. [Abstract] [Full Text] [PDF]