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Human Reproduction, Vol. 13, No. 10, 2731-2737, October 1998
© 1998 European Society of Human Reproduction and Embryology

Immunoneutralization of follicle stimulating hormone does not affect gonadotrophin surge-inhibiting factor/ attenuating factor bioactivity during the rat ovarian cycle

S. Tio, J.A.M.J. van Dieten and J. de Koning

Leiden Amsterdam Center for Drug Research, Division of Medical Pharmacology, University of Leiden, Sylvius Laboratories, Wassenaarseweg 72, 2333 AL Leiden, The Netherlands

Correspondence: To whom correspondence should be addressed

The physiological role of follicle stimulating hormone (FSH) in the regulation of the release of the putative ovarian factor gonadotrophin surge-inhibiting or -attenuating factor (GnSIF/AF) was investigated. Blood FSH concentrations were immunoneutralized in female rats during different days of the ovarian cycle. FSH antiserum was injected in different protocols to neutralize the FSH surge(s) and/or basal FSH concentrations. All animals were killed on the morning of the day of pro-oestrus of the control rats. Hemi-pituitaries were incubated and gonadotrophin-releasing hormone (GnRH) stimulated and basal luteinizing hormone (LH) and FSH releases and pituitary contents were measured. The biological effectiveness of the FSH antiserum was established by monitoring the histology of vaginal smears and inhibin concentrations in trunk-blood. The predominance of small leukocytes in the smears (low oestradiol bioactivity) and the decreased (bioactive) inhibin secretion imply that anti-FSH neutralizes FSH bioactivity. Simultaneously, the results showed that all anti-FSH injections did not affect the biphasic LH response to GnRH in-vitro, which shows an unaltered presence of GnSIF/AF bioactivity in the blood circulation. The results suggest that under physiological conditions GnSIF/AF bioactivity, which keeps the LH responsiveness of the pituitary gland suppressed to the action of GnRH, is not supported by inhibin and not controlled by FSH.

Key words: functional antagonism/GnRH/hyperstimulation/luteinizing hormone/self-priming


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