Age-related changes in the neuroendocrine (endocrine-paracrine) cell population and the serotonin content of the guinea pig prostate.

Neuroendocrine (endocrine-paracrine, APUD) cells of the guinea pig prostatic complex (prostate and coagulating gland) were studied at three age points (9-day-old weanlings, 11 to 12 week mature pre-breeders, and retired breeders) using serotonin immunocytochemistry for detection and subsequent morphometric analysis. Prostatic complex serotonin levels were determined for the same age groups using high performance liquid chromatography with electrochemical detection. The numbers of neuroendocrine (NE) cells in the prostatic complex of retired breeders was 1.42 +/- 0.29 NE cells/mm gland length (mean +/- SEM) and was increased nearly 24-fold when compared with mature pre-breeders with 0.06 +/- 0.03 NE cells/mm gland length and nearly 16-fold when compared with the weanlings with 0.09 +/- 0.04 NE cells/mm gland length. The increase in cell number in the retired breeders versus each of the other age groups was highly significant (p less than 0.001). The increase in NE cells appeared to take place exclusively in the prostate, whereas the number of NE cells in the coagulating gland were few and not significantly different in the three age groups. The number of urethral NE cells also appeared similar in all three age groups. The number of prostatic epithelial cells/gland length increased with age. The number of NE cells/100 prostatic epithelial cells was examined in the three age groups and the increase in retired breeders over the other two groups was still highly significant (p less than 0.001). Serotonin levels, which were measured for the whole prostatic complex, indicated a nearly 6-fold increase with age: retired breeders had 97.72 +/- 21.26 ng/g of wet tissue (mean +/- SEM) whereas mature pre-breeders had 17.1 +/- 2.88 ng/g of wet tissue (p less than 0.01). Weanling serotonin levels were not detectable. This dramatic age-related increase in prostatic NE cells and serotonin content could reflect a compensation for a decreased effectiveness of NE cell hormones, a nonfunctional primary hyperplasia, a hyperplasia secondary to endogenous hormonal or involutional changes or exogenous factors. Whatever the mechanism, this increase in prostatic NE cells with age is of great interest since human prostatic carcinoma and benign nodular hyperplasia are both strongly correlated with advanced age. Prostatic NE cells may, therefore, directly or indirectly be in the pathogenesis and/or evolution of these important pathologic processes.