Abstract
A variety of neurotransmitters and neuromodulators affect the activity of neurons synthesizing gonadotropin-releasing hormone (GnRH) in the hypothalamus, whereby regulate the release of gonadotropins from the anterior pituitary. Among them are prostaglandins which are synthesized by cyclooxygenages (COX) and are thought to be indispensable for the ovulatory surge of gonadotropins. The aim of the present study was to examine the effect of inhibition of prostaglandin synthesis on hypothalamic GnRH neurons prior to the expected ovulatory surge of gonadotropins. Ovariectomized rats were primed with estradiol benzoate (20 ;μg, sc) 3 days before the experiment, and were treated with progesterone (1 mg, sc) at noon on the day of experiment to reliably induce the gonadotropin surge. COX inhibitors, indomethacin (arylalkanoic acid class of NSAID; 8 mg/kg), flurbiprofen (2-Arylpropionic acid class of NSAID; 1mg/kg) or the vehicle was injected iv at noon. The rats were perfused with formaldehyde under deep anesthesia at 1700h. The brains were fixed and processed for double immunofluerescent staining against GnRH and c-Fos. The COX inhibitors significantly decreased the number of GnRH-immunoreactive cells in the hypothalamus. The result was in marked contrast to the effect of lipopolysaccharide which did not affect GnRH cell numbers but reduced c-Fos positive cells among them. These results suggest that prostaglandins may control GnRH synthesis in the hypothalamus. [J Physiol Sci. 2008;58 Suppl:S137]
