Mangels R A, Powers J B, Blaustein J D
Department of Psychology, University of Massachusetts, Amherst 01003-7710, USA.
Brain Res. 1998 Jun 15;796(1-2):63-74. doi: 10.1016/s0006-8993(98)00318-7.
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.
暴露于短光照周期的雌性叙利亚仓鼠对雌二醇和孕酮的行为反应性降低与神经甾体受体浓度的降低有关。研究了长光照周期和短光照周期（LP；SP）暴露对去卵巢仓鼠腹内侧下丘脑（VMH）、内侧结节区（mTu）、内侧视前区（mPOA）、杏仁核内侧核（mAMYG）和弓状核（ARC）中甾体受体免疫反应性的影响。在实验1中，暴露于短光照周期10周会减弱雌二醇和孕酮序贯处理后的脊柱前凸反应。在另一组未给予激素的动物中，短光照周期降低了内侧视前区雌激素受体免疫反应性（ERIR）细胞的染色强度，同时增加了部分杏仁核内侧核中可检测到的ERIR细胞数量。在实验2中，短光照周期如实验1那样减弱了脊柱前凸反应。一周后，对同一批雌性仓鼠进行全身注射雌二醇以诱导孕激素受体（PR）。饲养在短光照周期环境中的动物在腹内侧下丘脑（VMH）、内侧结节区（mTu）、内侧视前区（mPOA）、杏仁核内侧核（mAMYG）和弓状核（ARC）中显示出显著降低的孕激素受体免疫反应性（PRIR）。实验3研究了实验2的结果是否可能受到光照周期对雌二醇外周代谢影响的干扰。在饲养于长光照周期或短光照周期环境中的仓鼠中，通过单侧在下丘脑内侧基底部植入雌二醇来诱导孕激素受体，从而绕过光照周期对雌二醇外周可用性可能产生的影响。这种处理导致短光照周期雌性仓鼠腹内侧下丘脑（VMH）和内侧视前区（mPOA）中可检测到PRIR的细胞显著减少，这表明在实验2中观察到的光照周期对孕激素受体诱导的影响并不依赖于雌二醇外周可用性的改变。
