Analysis of mouse plus-maze behavior modulated by ovarian steroids
Analysis of mouse plus-maze behavior modulated by ovarian steroids
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DOI：
10.1016/s0166-4328(00)00341-7
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发表时间：
2001-02-15
影响因子：
2.7
通讯作者：
Tuohimaa, P
中科院分区：
文献类型：
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作者：
Galeeva, A;Tuohimaa, P
卵巢激素通过膜受体和核受体起作用，可引起受试者心理生理状态的不同变化。这种影响在雌性生物体中最为关键，因为卵巢激素会因发情周期而自然波动。在这项研究中，我们分析了雌激素和孕激素（P）如何影响卵巢切除（OVX）小鼠的焦虑水平。在十字迷宫实验中，我们发现注射孕酮6 h的小鼠，其开臂活动水平最低，梳理活动水平最高。用苯甲酸雌二醇（EB）处理的OVX动物的张开手臂和自发活动所花费的时间与溶剂处理的动物没有差异。此外，激素治疗改变了许多脑区的PR免疫反应性，如下丘脑内侧视前区，下丘脑腹内侧，下丘脑乳头体，隔海马区和导水管周围灰质。与溶剂处理的小鼠相比，EB和P的注射诱导PR-IR的连续变化，而溶剂的注射诱导PR-IR在所有检查的脑区中的显著降低。我们的数据表明，性类固醇激素在诱导焦虑中起着重要作用。此外，这种作用可能部分通过经典的类固醇受体介导。(C)2001 Elsevier Science B. V.保留所有权利。
Ovarian hormones, acting through membrane and nuclear receptors, can evoke different changes in psychophysiological status of the subject. Such effects are most crucial in female organism because of the natural fluctuations of ovarian hormones due to the estrous cycle. In this study, we have analyzed how estrogen and progesterone (P) affect the anxiety level in ovariectomized (OVX) mice. Using plus-maze paradigm, we have found that mice receiving injection of progesterone in 6 h revealed the lowest level of open arm activity and the highest grooming activity, as compared with other experimental groups. Time spent on the open arms and locomotor activity of OVX animals treated with estradiol benzoate (EB) did not differ from the vehicle-treated animals. In addition, the hormonal treatments modified the PR-immunoreactivity in many brain areas, such as medial preoptic area of hypothalamus, ventromedial hypothalamus, mammilar body of hypothalamus, septo-hippocampal region, and periaqueductal gray. The injections of EB and P induced sequential changes of PR-ir in comparison with vehicle-treated mice, whereas injection of vehicle induced the significant decrease of PR-ir in all brain areas examined. Our data suggest that sex steroid hormones play an important role in induction of anxiety. Furthermore, this action might be partially mediated through the classical steroid receptors. (C) 2001 Elsevier Science B.V. All rights reserved.