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Brain-derived neurotrophic factor (BDNF) is a growth factor belonging to the family of neurotrophins. Although neurotrophins in the male genital organs have been well documented, their role in the biology of these organs is far from clear. In particular, little is known about the influence of sex hormones on neurotrophin expression. In the present study, using immunohistochemistry and enzyme-linked immunosorbent assay (ELISA), we investigated the distribution and tissue concentration of BDNF in the vas deferens and accessory male genital glands in normal and castrated rats. The expression of BDNF mRNA was also investigated. In normal rats, BDNF immunoreactivity was localized in the musculature of the vas deferens and vesicular gland and in the fibromuscular stromal cells of the prostate. In the ventral prostatic lobes, BDNF immunoreactivity was localized in basal, secretory and neuroendocrine epithelial cells. Innervating ganglia and nerves were immunoreactive in all the examined tracts. After castration, BDNF immunoreactivity increased in the musculature of the vesicular gland and in the fibromuscular stromal cells of both dorsal and ventral prostatic lobes. BDNF immunoreactivity also increased in the nerves. ELISA and reverse transcription/real-time polymerase chain reaction confirmed the findings of the immunohistochemical study. In the accessory glands, castration induced an increase of both BDNF tissue concentration and mRNA expression. These results suggest that BDNF is expressed in the internal male genital organs of the rat and that its expression is downregulated by androgen hormones. We hypothesize that the observed BDNF increases are related to the castration-induced regression of the sympathetic nerves.

The influence of chronic maternal morphine on the parvalbumin immunoreactive patterns in developing mouse brain was studied. Female Swiss mice were administered daily saline or morphine (30 or 60 mg/kg) for a period of 7 days before mating, gestation, and 21 days postpartum. Their pups were sacrificed on postnatal day 18 and the brains were examined histologically and immunohistochemically for parvalbumin-positive neurons. Histological observations revealed no significant changes in the cell number of the morphine-exposed neonatal forebrain, whereas the number of parvalbumin-positive neurons increased in layers II-IV of the parietal cortex I. Moreover, the number of parvalbumin-positive dendrites increased remarkably in the cingulate and parietal I cortices of the morphine-exposed neonates, indicating the region-specific increase in the PV immunoreactive profiles. These results are consistent with the key roles played by the above brain regions in the altered behavioral patterns of the maternally addicted neonates, such as impaired somatosensory and cognitive performances. The mechanism of morphine action on parvalbumin expression in neonatal mouse brain is not evident, but alterations in the expression patterns of parvalbumin in specific regions of the developing brain might be one of the cellular mechanisms by which addictive drugs modify the functional aspects of the developing CNS.

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