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Endocrinology Vol. 138, No. 3 1008-1013
Copyright © 1997 by The Endocrine Society

Articles

Inhibition of Gonadotropin-Induced Testosterone Secretion by the Intracerebroventricular Injection of Interleukin-1ß in the Male Rat1

Andrew V. Turnbull and Catherine Rivier

The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037

Address all correspondence and requests for reprints to: Catherine Rivier, Ph.D., The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, 10010 North Torrey Pines Road, La Jolla, California 92037. E-mail: Crivier{at}salk.edu

The intracerebroventricular (icv) injection of the proinflammatory cytokine interleukin (IL)-1ß is known to significantly decrease plasma LH levels in the male rat, thereby lowering testosterone (T) secretion. We show here that central administration of this cytokine (20–80 ng) also inhibits T secretion in response to human CG (hCG), an effect that is apparent already when IL-1ß is injected 15 min before hCG. This phenomenon is independent of LH secretion because lowering LH levels with the potent GnRH antagonist Azaline B neither mimics nor affects the suppressive influence of icv IL-1ß on the hCG-induced T secretory response. Elevations in plasma corticosterone levels do not seem to play a role either, because icv IL-1ß is able to blunt hCG-induced T secretion in animals whose corticosterone has been removed by adrenalectomy or reduced by the administration of antibodies to CRF. Furthermore, the observation that icv IL-1ß inhibits the T response to hCG before elevations in plasma IL-6 concentrations are detectable, and that central treatment with the cytokine is more effective than iv treatment, indicates that circulating levels of neither IL-1ß nor IL-6 are important mediators of this effect. Collectively, these results lead us to propose that IL-1ß of central origin influences neural pathways linking the brain and the testes, resulting in decreased testicular responses to hCG.




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