Molecular species of prostaglandins involved in modulating luteinizing hormone pulses of female rats under infectious stress conditions

Abstract

Mammalian reproductive function is controlled by the hypothalamus-pituitary-gonadal (HPG) axis, which is suppressed under infectious stress conditions. We have previously demonstrated, by analyzing the pulsatility of luteinizing hormone (LH), that prostaglandins (PGs) in the central nervous system (CNS) mediate infectious stress to suppress the activity of the HPG axis. The aim of the present study is to characterize the types of PGs responsible for suppression of the HPG axis. We focused on 3 major types of PGs, i.e., PGE₂, PGD₂, and PGF_2α. We used female rats overiectomized bilaterally 1 week before the experiments. Lipopolysaccharide (LPS, 100 μg/kg) suppressed LH pulses while enhancing the concentration of all 3 PGs in the CSF, which was restored by indomethacin (10 mg/kg). Subsequently, we observed LH pulsatility after a single injection of each PG and after co-injection of PGE₂ with PGF_2α into the third cerebral ventricle. A single injection of PGE₂ dose-dependently induced a transient increase in mean LH concentration and LH pulse amplitude, and PGD₂ significantly increased the amplitude of LH pulses, while PGF_2α did not affect LH pulsatility. On the other hand, co-injection of PGE₂ and PGF_2α induced significant suppression of both frequency and amplitude of LH pulses. These results suggest that PGE₂ and PGF_2α can be one of the mediators that suppress the HPG axis in situations of infectious stress. Moreover, they imply that there are 2 contradictory effects of PGE₂ on LH pulsatility: enhancive when working alone while suppressive when working together with PGF_2α. (244/250)

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