The role of corticotropin-releasing factor (CRF) and opiocortin neuronal systems and a possible functional relationship between the two in the control of luteinizing hormone-releasing hormone (LH-RH) activity in the medial preoptic area (MPOA) for the regulation of lordosis behaviour were assessed in ovariectomised oestrogen-progesterone-treated female rats. Lordosis behaviour (assessed as the lordosis quotient) triggered by male mounting was significantly inhibited by either CRF or beta-endorphin infused into the MPOA in animals treated with normal doses of oestradiol benzoate (OEB) (5 micrograms) and progesterone (500 micrograms). Saline-treated animals exhibited high levels of lordosis. The inhibition of lordosis produced by either CRF or beta-endorphin could be reversed by LH-RH microinfusions into the MPOA. While naloxone pretreatment of the MPOA site prevented the inhibitory effects of beta-endorphin, neither the opiate antagonist nor anti-beta-endorphin-gamma-globulin (even in high concentrations) infused into the MPOA was effective in completely preventing the inhibition of lordosis produced by CRF. These findings suggest that the inhibition of LH-RH neuronal activity and lordosis behaviour by CRF may be due to a direct action and may not be the result of activation of beta-endorphin release. The possibility that the two peptidergic systems may act in a synergistic fashion is supported by the data showing that combined CRF-beta-endorphin treatment in the MPOA completely abolished lordosis. This is further supported by the finding that CRF totally abolished lordosis in animals pretreated with anti-corticotropin (ACTH-gamma-globulin although this result could suggest that CRF could preferentially stimulate the release of ACTH in the MPOA.(ABSTRACT TRUNCATED AT 250 WORDS)