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Vasopressin (VP) neurons in the bed nucleus of the stria terminalis (BNST) are steroid sensitive and sexually dimorphic. The number of VP messenger RNA (mRNA)-expressing neurons is larger in male than in female rats. This initial observation suggested that sexual dimorphism resulted from enhanced proliferation and/or survival of VP neurons after gonadal hormone exposure during the critical perinatal period. However, galanin (GAL) and VP mRNAs were recently reported to be coexpressed in the BNST of adult male rats, and GAL gene expression, unlike VP gene expression, is not sexually dimorphic. These findings are consistent with the hypothesis that the sex difference in VP cell number in the BNST results from a sex difference in the number of GAL neurons dedicated to express the VP gene. To test this hypothesis, double in situ hybridization histochemistry was performed for GAL and VP mRNAs in the BNST of adult male and female rats. For quantification, the posterior BNST was divided into its two anatomical regions: medial (BSTM) and lateral (BSTL) divisions. Extending previous results for the whole BNST, the number of GAL-expressing cells in either the BSTM or the BSTL was not sexually dimorphic. A significant sex difference was found in the number of GAL cells coexpressing VP in the BSTM (mean +/- SE, male, 124 +/- 8; female, 56 +/- 6; P < or = 0.0001), but not in the BSTL (male, 80 +/- 9; female, 83 +/- 15). Accordingly, the number of cells expressing GAL mRNA only was significantly lower (P < or = 0.002) in the BSTM of male (43 +/- 5) than in female (85 +/- 9) rats. Evidence is provided that the reduced incidence of coexpression of VP by GAL neurons in the BSTM of female rats may account for the reported sex difference in VP cell number in the entire BNST. The results suggest that gonadal hormones in the perinatal period may not influence the proliferation and/or survival of VP neurons in the BNST per se but influence, instead, the capacity of GAL neurons to synthesize VP.

The sensitivity of hypothalamic centers to estrogenic regulation may be impaired with age and contribute to the loss of reproductive function in female rats. Here, we have tested the hypothesis that aging is associated with alterations in the level of expression of the estrogen receptor (ER) gene and/or the neurotensin/neuromedin-N (NT/N) gene in the preoptic area (POA) of female rats. We have used in situ hybridization histochemistry and quantitative autoradiography to compare ER gene expression and NT/N gene expression in the POA of ovariectomized and ovariectomized/estradiol-treated female rats at 3, 11, and 20 months of age. We found no evidence for an age-related impairment of either ER or NT/N gene expression in two subdivisions of the POA: the anterior medial preoptic nucleus and the medial preoptic nucleus. Likewise, estrogenic regulation of both ER messenger RNA levels and NT/N messenger RNA levels did not differ across age groups. These results indicate that transcription of the ER gene within the POA is not reduced with age and suggest that the receptor translated within the POA functions normally in old female rats. Our observations do not support a role for impaired expression of the ER gene or impaired estrogenic induction of NT/N gene expression by preoptic neurons in the development of reproductive acyclicity with aging.

Neurons in the bed nucleus of the stria terminalis (BNST) and the medial amygdala (AMe) coexpress vasopressin and galanin (GAL) in the adult male rat. Here, we have asked whether GAL gene expression, like vasopressin gene expression in these same neurons, exhibits sexual dimorphism and whether GAL pathways in the BNST and AMe are activated with puberty in female rats as we have previously observed in male rats. In Exp 1, in situ hybridization histochemistry and quantitative autoradiography were used to compare GAL gene expression in the BNST and AMe of prepubertal (24-day-old) and adult (90-day-old) male and female rats. In the BNST, both the number of GAL mRNA-expressing neurons (F = 41.98; P < or = 0.0001; males, P < or = 0.007; females, P < or = 0.001) and the intensity of labeling (F = 40.35; P < or = 0.0001; males, P < or = 0.004; females, P < or = 0.002) were significantly increased in adult compared to prepubertal animals of both sexes. In the AMe of both males (P < or = 0.001) and females (P < or = 0.001), the intensity of labeling was significantly enhanced across puberty (F = 66.29; P < or = 0.0001); however, the number of GAL mRNA-expressing neurons in this region did not change. We found no evidence for sexual dimorphism of GAL gene expression in either brain region. In Exp 2, we replicated our observations of a lack of sexual dimorphism of GAL gene expression in the BNST of adult male and female rats. These findings are consistent with the hypothesis that GAL neurons in the BNST and AMe are steroid sensitive in both sexes. However, our failure to detect any differences in either the number of GAL mRNA-expressing neurons or the level of expression between male and female rats at either age indicates that these pathways do not exhibit sexual dimorphism.