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K. YAMANOUCHI and Y. ARAI

Department of Anatomy, Juntendo University School of Medicine, Hongo, Tokyo 113, Japan

(Received 18 October 1977)

Differentiation of sexual behaviour patterns in male rats is dependent on the internal secretion of the testes during neonatal life. Removal of the testes at this time causes feminization and results in male rats which display female patterns of sexual behaviour (Gorski, 1971). Female patterns of behaviour are usually rare in normal male rats but recently we found that transection of the dorsal afferent neurones to the preoptic and anterior hypothalamic areas potentiated the display of lordosis in hormonally primed male rats (Yamanouchi & Arai, 1975). In the present study, further neuroanatomical analysis was carried out to clarify the localization of the afferent pathway involved in the regulation of lordosis behaviour.

Anterior or posterior roof deafferentation (ARD or PRD) was performed by lowering an L-shaped Halasz knife (2-5 mm horizontal blade) to the level

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T Matsuwaki, M Suzuki, K Yamanouchi, and M Nishihara

We have previously reported that tumor necrosis factor-alpha (TNF-alpha) suppressed pulsatile secretion of luteinizing hormone (LH) in adrenalectomized (ADX) rats, which was restored by replacement of glucocorticoid. In the present study, we examined the role of glucocorticoid in inducing the preovulatory LH surge under conditions of infectious stress. Intravenous injection of TNF-alpha (1 microg) into the proestrous rats at 1300 h attenuated the LH surge and decreased the number of oocytes ovulated. The inhibitory effect of TNF-alpha on the LH surge was blocked by pretreatment with indomethacin, suggesting that the effects of TNF-alpha were mediated by prostaglandins (PGs). On the other hand, ADX markedly enhanced the inhibitory effect of TNF-alpha on the LH surge and subsequent ovulation, which was almost completely restored by pretreatment with a subcutaneous injection of corticosterone (10 mg). These results suggest that glucocorticoid counteracts the inhibitory effect of the cytokines on the preovulatory LH surge by suppressing PG synthesis, and thereby helps to maintain reproductive function under infectious stress conditions.