Plasma prolactin concentrations and testicular human chorionic gonadotropin binding sites during short photoperiod-induced testicular regression and recrudescence in the golden hamster.

Abstract

Experiments were conducted in the golden hamster to determine temporal relationships and statistical correlations between plasma PRL concentrations and unoccupied testicular hCG binding sites during short photoperiod-induced testicular regression and spontaneous recrudescence. Although two experiments provided statistically significant (P<O.02) correlations between plasma PRL concentrations and testicular hCG binding, variability in onset of increased plasma PRL during recrudescence prevented any definite conclusions concerning a possible cause-and-effect relationship. Hence, the data do not indicate that a period of increased PRL secretion either initiates, or is initially necessary for, spontaneous recrudescence or changes in testicular hCG binding occurring during spontaneous recrudescence. Time of initiation of spontaneous testicular recrudescence was variable, but was always associated with increases in plasma concentrations of LH, FSH, and PRL. Testes from hamsters maintained in either short or long photoperiod had a single class of high affinity hCG binding sites with an average equilibrium association constant (Ka) of 3.06 × 1010 M−1. During the first 4 weeks of short photoperiod, when no changes in testicular weights were found, there were significant decreases in both concentration (fmol/mg protein) and total content (fmol/testes) of testicular hCG binding sites. However, after 10 weeks of short photoperiod and continuing through 16–18 weeks, the concentration of hCG binding sites was increased, while total content remained depressed, in regressed testes when compared with testicular hCG binding found in long photoperiod hamsters. Use of either [125I] iodo-hCG or [125I] iodo-hLH gave identical results. This increased concentration of unoccupied hCG/hLH binding sites may represent 1) an increase in binding sites per Leydig cell; 2) decreased occupancy or decreased loss of testicular hCG binding sites commensurate with decreased plasma LH concentrations; or 3) a relative increase in numbers of Leydig cells compared with other testicular components as testes undergo regression.