Effect of photoperiod on neural estrogen and progestin receptor immunoreactivity in female Syrian hamsters.

This study explored the possibility that reduced behavioral responsiveness to estradiol and progesterone in female Syrian hamsters exposed to a short photoperiod is associated with a reduction in the concentration of neural steroid receptors. The effects of long and short photoperiod (LP; SP) exposure on steroid receptor immunoreactivity were examined in the ventromedial hypothalamus (VMH), medial tuberal region (mTu), medial preoptic area (mPOA), medial nucleus of the amygdala (mAMYG), and the arcuate nucleus (ARC) of ovariectomized hamsters. In Experiment 1, exposure to SP for ten weeks attenuated the lordosis response following sequential treatment with estradiol and progesterone. In a separate group of animals not given hormones, SP decreased the staining intensity of estrogen receptor immunoreactive (ERIR) cells in the mPOA while increasing the number of detectable ERIR cells in part of the mAMYG. In Experiment 2, SP diminished the lordosis response as it did in Experiment 1. One week later, the same females were administered estradiol systemically to induce progestin receptors (PR). Animals housed in SP showed significantly reduced progestin receptor immunoreactivity (PRIR) in the VMH, mTu, mPOA, mAMYG, and ARC. Experiment 3 examined whether the results of Experiment 2 might have been influenced by photoperiodic effects on peripheral metabolism of estradiol. Among hamsters housed in LP or SP, PRs were induced by estradiol implanted unilaterally in the medial basal hypothalamus, thus bypassing possible photoperiodic effects on peripheral estradiol availability. This treatment resulted in significantly fewer cells with detectable PRIR in the VMH and mPOA of SP females, suggesting that the photoperiodic influences on PR induction observed in Experiment 2 do not depend on alterations in the peripheral availability of estradiol.