The present study was undertaken to evaluate the role and possible interaction of the endogenous opioid peptide (EOP) and corticotropin‐releasing factor (CRF) in the acute stress‐induced suppression of gonadotropin secretion in ovariectomized estrogen‐primed rats. An intravenous (i.v.) injection of naloxone (10 or 20 mg/kg), an EOP antagonist, significantly elevated serum luteinizing hormone (LH) levels within 10 min in non‐stressed animals. The naloxone‐induced LH release was completely eliminated when tested 30 min after the onset of acute immobilization. In a subsequent study, it was found that suppression of the naloxone‐induced LH release occurred as early as 5 min after the stress onset, and was still evident 60 min after the end of a 30‐min period of immobilization. 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 μg) also significantly suppressed, in a dose‐related manner, the effect of a subsequent i.v. injection of naloxone. However, an i.c.v. injection of α‐helical CRF(9‐41) (25 or 50 μg), a CRF antagonist, prior to immobilization, could not interfere with the suppressive effect of stress on naloxone‐induced LH release. These results suggest that both acute immobilization stress and CRF can inhibit the LH secretory activity without mediation by EOP neurons. However, the stress‐related suppression may involve non‐CRF mechanism(s).
Journal of Neuroendocrinology – Wiley
Published: Aug 1, 1996
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