Km. Tahka et al., HORMONAL AND PHOTOPERIOD-INDUCED CHANGES IN TESTICULAR INTERLEUKIN-1-LIKE FACTOR IN BANK VOLES, CLETHRIONOMYS-GLAREOLUS, Journal of Reproduction and Fertility, 97(2), 1993, pp. 469-474
Testicular interleukin-1-like factor (tIL-1) is a cytokine secreted pr
esumably by Sertoli cells in several mammalian species. The function o
f this cytokine is unknown: tIL-1 may control meiosis, act as a mitoge
n for spermatogonia or have both of these functions. The present inves
tigation was conducted to assess tIL-1 activity and its hormonal contr
ol in a seasonally breeding photoperiodic mammal during testicular mat
uration and photoperiod-induced regression. Testicular maturation in l
ong photoperiod (20 h light:4 h dark) was accompanied by the appearanc
e of tIL-1 activity at the age of 32-39 days which increased as full s
exual maturity was reached. No significant tIL-1 activity was detected
when pubertal development was inhibited or testicular regression indu
ced by subjecting juvenile and adult bank voles to a short photoperiod
(6 h light: 18 h dark) for 6 to 8 weeks. Administration of human chor
ionic gonadotrophin (hCG; 60 iu kg-1) increased tIL-1 activity in sexu
ally mature as well as regressed testes. In the photoregressed voles F
SH (1.2 U kg-1) administration, which induced a three-fold increase in
testicular weight and stimulated spermatogenesis, did not induce dete
ctable concentrations of tIL-1. Administration of FSH followed by hCG
increased tIL-1 activity significantly in the atrophic testis, but thi
s was probably due to hCG, since FSH treatment alone was without effec
t. In conclusion, in accordance with the proposed role of tIL-1 as a g
erm-cell mitogen and a meiosis-promoting factor, tIL-1 activity correl
ated positively with spermatogenic activity during testicular maturati
on and photoperiod-induced regression. IL-I production may depend on L
H but not FSH. In bank voles and possibly other photosensitive seasona
l breeders, photoperiod modulates the production of tIL-1 indirectly t
hrough the neuroendocrine system.