PATTERN OF FOS AND JUN EXPRESSION IN THE FEMALE RAT FOREBRAIN AFTER SEXUAL-BEHAVIOR

Previous studies indicated that sexual behavior in female rats primed with estradiol and progesterone induced expression of the immediate early gene (IEG) c-Fos in various brain areas rich in estradiol receptors, including the medial preoptic area (MPA), the medial amygdala (AMe), and the ventromedial nucleus of the hypothalamus (VMN), and to a lesser extent areas with low densities of estradiol receptors, such as the caudate nucleus, the dentate gyrus and the cingulate cortex. The goal of the present experiment was to compare this pattern of expression with the distribution of other IEG products within the Jun family, The results indicate that in non-mated animals, Jun-B, c-Jun and Jun-D were differentially present in several forebrain areas. As previously reported for c-Fos, there was little effect of estradiol and progesterone treatment on the brain expression of these Jun proteins. The most striking result was that sexual behavior stimulated expression of Jun-B and c-Jun, but not Jun-D, in areas containing high densities of estradiol receptors. Specifically, after sexual behavior the MPA and the bed nucleus of the stria terminalis co-expressed c-Fos, Jun-B, c-Jun. c-Fos was co-induced with Jun-B in the VMN, and with c-Jun in the AMe. In contrast, there was no detectable increase in Jun-B, c-Jun or Jun-D in either the caudate nucleus, dentate gyrus or cingulate cortex after sexual behavior, although these regions expressed weak to moderate levels of either Jun-B, c-Jun, or Jun-D basally. Thus, the presence of estradiol receptors coincides with the co-expression of Fos and Jun proteins after sexual behavior. The biological basis for the differential expression of AP-1 components in various brain areas after sexual behavior may reside in either the cellular phenotypes or the neurochemical afferent stimulation invoked by sexual behavior in these brain areas. These differences in IEG expression, in turn, may contribute to differential regulation of gene expression.