ACUTE IMMOBILIZATION STRESS AND INTRAVENTRICULAR-INJECTION OF CRF SUPPRESS NALOXONE-INDUCED LH-RELEASE IN OVARIECTOMIZED ESTROGEN-PRIMED RATS

The present study was undertaken to evaluate the role and possible int eraction of the endogenous opioid peptide (EOP) and corticotropin-rele asing factor (CRF) in the acute stress-induced suppression of gonadotr opin secretion in ovariectomized estrogen-primed rats. An intravenous (i.v.) injection of naloxone (10 or 20 mg/kg), an EOP antagonist, sign ificantly elevated serum luteinizing hormone (LH) levels within ID min in non-stressed animals. The naloxone-induced LH release was complete ly eliminated when tested 30 min after the onset of acute immobilizati on, In a subsequent study, it was found that suppression of the naloxo ne-induced LH release occurred as early as 5 min after the stress onse t, and was still evident 60 min after the end of a 30-min period of im mobilization. The effect of naloxone was restored 3 h after liberation of the animal from the 30-min immobilization. An intraventricular (i. c.v.) injection of CRF (1 or 5 mu g) also significantly suppressed, in a dose-related manner, the effect of a subsequent i.v. injection of n aloxone, However, an i.c.v. injection of alpha-helical CRF(9-41) (25 o r 50 mu g), a CRF antagonist, prior to immobilization, could not inter fere with the suppressive effect of stress on naloxone-induced LH rele ase, These results suggest that both acute immobilization stress and C RF can inhibit the LH secretory activity without mediation by EOP neur ons, However, the stress-related suppression may involve non-CRF mecha nism(s).