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Glucocorticoid Maintains Pulsatile Secretion of Luteinizing Hormone under Infectious Stress Condition

Department of Veterinary Physiology, Veterinary Medical Science, The University of Tokyo, Tokyo 113-8657, Japan

Address all correspondence and requests for reprints to: Masugi Nishihara, Ph.D., D.V.M., Department of Veterinary Physiology, Veterinary Medical Science, The University of Tokyo, Tokyo 113-8657, Japan. E-mail: amnishi{at}mail.ecc.u-tokyo.ac.jp.

We have previously shown that TNF-, a major proinflammatory cytokine, suppressed hypothalamic GnRH pulse generator activity and that this inhibitory effect was enhanced by -helical CRH, a CRH receptor antagonist. The present study was conducted to elucidate the involvement of glucocorticoid (GC) in modulating LH pulses under infectious stress condition. Adrenalectomy (ADX) markedly enhanced the suppressive effect of TNF- (1 µg), injected iv, on LH pulses in ovariectomized (OVX) rats. Pretreatment with a sc injection of corticosterone (10 mg) almost completely restored LH pulses after TNF- injection in OVX/ADX animals. Injection of TNF- increased the number of c-Fos-immunoreactive cells in the supraoptic nucleus (SON), the dorsomedial hypothalamic nucleus (DMH), and the parvocellular region of the paraventricular nucleus (PVN), which was more prominent in OVX/ADX than OVX animals except in the DMH. Pretreatment with corticosterone decreased the number of Fos-immunoreactive cells in the PVN and SON but not in the DMH. These results suggest that GC has a potent protective effect on LH pulsatility under conditions of infectious stress, the mechanism of which involves at least the suppression of the excitability of PVN and SON neurons. In addition, the DMH does not seem to mediate the central action of GC, though it may play an important role in inducing pathophysiological reactions to invasive stress.

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