In order to ascertain the influence of gonadal steroid hormones on the secretory response of the hypothalamic-hypophyseal luteinizing hormone (LH) axis to acute stress, the effects of four specific stressors on LH release were compared in ovariectomized versus ovariectomized steroid-treated rats. Groups of adult female Copenhagen-Fischer 344 rats were ovariectomized for either 1 or 2 weeks and exposed for specific intervals to one of the following stressors: novel environment, strobe light, restraint, or swim. Additional groups of animals were ovariectomized for 2 weeks and injected with 10 µg estradiol benzoate 24 and 48 h prior to exposure to the same stress stimuli. Multiple blood samples were obtained from these and nonstressed experimental controls at specific time points before, during, and after stress exposure. Transfer of 1-week ovariectomized rats to a novel environment, followed by a return to their original quarters 30 min later, resulted in a well-defined pattern of increased LH release. Novel environment stress also stimulated LH release in 2-week ovariectomized rats, as indicated by the comparison of mean LH values from the pre-stress versus post-stress sampling periods by paired t test. Strobe light stress, on the other hand, had no effect on circulating LH in 1-week ovariectomized rats, but significantly increased mean post-stress plasma LH levels compared to mean pre-stress values in 2-week ovariectomized rats. While exposure to either 15 min of restraint or 10 min of swim stress had no effect on LH in rats ovariectomized for 1 week, both of these stressors resulted in a marked decline in LH release in 2-week ovariectomized animals. Circulating LH returned to pre-stress values by 45 min after initiation of restraint, but hormone levels remained suppressed after swim stress until the end of the experiment (60 min). The administration of naltrexone (NALT), an endogenous opiate receptor antagonist, effectively reversed the inhibitory effect of both restraint and swim on LH release in 2-week ovariectomized rats and resulted in a greater elevation in plasma LH in both groups of stressed rats compared to that observed in nonstressed NALT-treated animals. Ovariectomized estrogen-treated rats showed no alterations in LH release during exposure to either novel environment, strobe light, or swim stress. Restraint stress, on the other hand, resulted in a temporary, but significant elevation in circulating LH, detectable at both 10 and 25 min after onset of stress. Hormone values returned to pre-stress levels by 45 min after time zero. The results of the present study demonstrate that several acute stressors can elicit, under uniform experimental conditions, differential alterations in LH release and that these disparate hormonal responses may depend, in part, upon the animal’s gonadal steroid milieu. These findings suggest that specific stressors may influence LH release via individual mechanisms rather than a common pathway and support the view that gonadal steroid hormones fulfill an important modulatory role in the responsiveness of the hypothalamic-hypophyseal LH axis to a variety of acute stress stimuli. The current data also indicate that ovariectomy can result in time course related alterations in the LH response to specific stressors. From the present work, that NALT-induced reversal of the suppressive effect of both restraint and swim stress on LH release in 2-week ovariectomized rats suggests that endogenous opioid peptides may be involved in central inhibitory mechanisms activated by these two stressors in the gonadectomized animal.

Keywords:
Luteinizing hormone, Stress, Estrogen, Endogenous opioid peptides, Naltrexone
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© 1988 S. Karger AG, Basel
1988
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