The present study was undertaken to analyze the changes in neuroendocrine cells of the human prostate induced by neoplasms and the effect of hormonal treatment. Samples of human prostate (n = 47) were obtained during surgery or removal of organs for transplantation. The cases analyzed represent normal prostates (n = 4); benign prostatic hyperplasias (n = 10; prostatic carcinomas with Gleason scores of 2-4 (n = 5), 5–7 (n = 10), and 8–10 (n = 3), and prostatic carcinomas treated with hormonal therapy (n = 15). Immunohistochemistry for chromogranin A was performed, and the density of neuroendocrine cells as well as the intensity of the immunostaining within their cytoplasms were evaluated using image analysis. Neuroendocrine cells showing chromogranin A immunoreactivity were identified in all cases studied. They were localized scattered in the acini, and no differences in their morphology were observed among groups. Interestingly, chromogranin A immunoreactivity was also present in typical epithelial cells of prostatic cancer with Gleason scores ranging from 8 to 10. The density of chromogranin A immunoreactive cells was higher in neoplastic tissue with respect to the normal prostate, reaching maximal values in prostatic carcinomas with Gleason scores of 8–10 which were hormonally treated. Regarding the intensity of immunostaining in the prostatic carcinomas with Gleason scores of 8–10 only, a significant increase in relation to the other groups was found. The present results demonstrate that the neuroendocrine cells have similar morphological features and distribution in normal prostate, benign prostatic hyperplasia, and prostatic carcinoma. Their density in prostatic cancer increases following hormonal therapy and varies in relation to the tumoral degree or histological evaluation, suggesting a role of neuroendocrine cells in human prostatic cancer.

Neurotrophins acting through Trk signal-transducing receptors play essential roles in the nervous system, and probably in some nonneuronal tissues. In the present study we used Western-blot and immunohistochemistry to investigate the occurrence and cellular localization of TrkB in the mouse kidney. Furthermore, the structure and ultrastructure of the kidney in mice carrying a mutation in the trkB gene were analyzed. TrkB in the kidney was identical to the cerebral one (145 kDa). Since the antibody used recognize a sequence within the tyrosine-kinase domain of TrkB, the renal TrkB receptor identified here must be regarded as able to mediate biological effects of their ligands. TrkB immunoreactivity was restricted to the juxtaglomerular apparatus, including differentiated vascular cells and extaglomerular mesangial cells. In these cells, TrkB colocalized with renin. The structural analysis revealed no major changes in the kidney structure of TrkB-deficient mice, with the exception of a significant reduction of the glomerular area. Nevertheless, in these animals there was an apparent increase in the number of extraglomerular mesangial cells (which retain the ability to synthesize renin) and absence of the macula densa. Taken together, these results strongly suggest a role of TrkB and their ligands in the control of the normal development and maintenance of the juxtaglomerular apparatus.

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