Abstract

The effect of N-methyl-D,L-aspartate (NMA) on LH secretion was investigated in Syrian hamsters of the LSH/Ss Lak strain, maintained under either long days (14 h of light, 10 h of darkness) or short days (6 h of light, 18 h of darkness). After 6 weeks of photoperiodic treatment, the animals were orchidectomized. Ten days later, 10-min blood samples were remotely collected from each animal, using surgically implanted intraatrial catheters, and individual pulsatile LH release profiles were subsequently determined by RIA. At the end of the 4-h sampling period, NMA was administered iv (30 mg/kg BW), and the LH response was determined in the next three plasma samples. Hamsters maintained under long days had very high mean plasma LH levels (453 +/- 46 ng/ml) and displayed episodic release patterns characterized by high amplitude pulses. In marked contrast, hamsters that were maintained under short days had significantly (P less than 0.001) lower mean plasma LH levels (90 +/- 12 ng/ml) and showed a significantly (P less than 0.001) lower mean pulse amplitude. The interpulse interval was similar in both of the groups, with LH peaks occurring, on the average, once every 65 min. When challenged with NMA, the long-day hamsters showed only a 37% increase in mean plasma LH levels, which was not statistically significant. In contrast, the short-day hamsters showed a highly significant (P less than 0.01) increase of 294%. Interestingly, the mean plasma LH levels after NMA administration were the same in the two photoperiodic groups despite a marked difference in the plasma levels that preceded the administration. These findings demonstrate that short days can inhibit the neuroendocrine activity of the hamster's reproductive axis independently of gonadal influences. They also suggest that the LHRH neurons have an intrinsic capacity to secrete very high levels of the neuropeptide, regardless of the photoperiod. Taken together, the results support the hypothesis that the breeding season in the hamster is regulated by a gonad-independent mechanism involving a photoperiodic modulation of neuroexcitatory inputs to the LHRH neurons.

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