Lordosis-enhancing medial preoptic area lesions do not alter hypothalamic estrogen receptor- or progestin receptor-immunoreactivity in prepubertal female guinea pigs

Abstract

Female guinea pigs rarely display adult-typical lordosis responses to ovarian steroid hormones until 40–50 days of age. Behavioral hyporesponsiveness in prepubertal females may be due, in part, to deficiencies in hypothalamic estrogen receptors and/or estradiol-induced progestin receptors. This study was designed to test the hypothesis that bilateral medial preoptic area (MPOA) lesions, which enhance the display of progesterone-facilitated lordosis in juvenile females, increase levels of hypothalamic estrogen receptors and/or estradiol-induced progestin receptors. Hartley guinea pigs were ovariectomized at 11–12 days of age and at 14–15 days of age received bilateral electrolytic or sham lesions aimed at the MPOA. At approximately 3 weeks of age, lesioned and sham-lesioned animals were either tested for the display of progesterone-facilitated lordosis or perfused, and their hypothalamic tissue processed for estrogen receptor- or estradiol-induced progestin receptor-immunostaining. Although a significantly higher percentage of MPOA-lesioned than sham-lesioned guinea pigs displayed progesterone-facilitated lordosis (85.7% vs. 5.8%, respectively, p<0.05), there were no significant lesion-related differences in the number or staining intensity of cells containing estrogen receptor- or estradiol-induced progestin receptor-immunoreactivity in the ventrolateral hypothalamus or arcuate nucleus. These data do not support the hypothesis that the enhanced display of progesterone-facilitated lordosis in prepubertal guinea pigs following MPOA lesions is due to increased hypothalamic concentrations of estrogen receptors or estradiol-induced progestin receptors.