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Biology of Reproduction, Vol 25, 536-548, Copyright © 1981 by Society for the Study of Reproduction
1 Department of Obstetrics and Gynecology,
The University of Texas Health Science Center at San Antonio,
San Antonio, Texas 78284 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 x 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.
2 Worcester Foundation for Experimental Biology,
Shrewsbury, Massachusetts 01545
Note:
ACKNOWLEDGMENTS
The authors wish to thank NIAMDD and Dr.
Robert Canfield for the hCG and hLH used in binding
studies, and Mrs. Mary Pat Hogan for performing the
testosterone radioimmunoassays. We are also grateful
to Dr. Robert Ryan for helpful suggestions during the
development of the hCG binding assay and to Dr.
Howard J. Brinkley for his helpful critique of this
manuscript.
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