Estrogen-dependent and estrogen-independent effects of progesterone on the electrophysiological excitability of dorsal midbrain neurons in golden hamsters.
Estrogen-dependent and estrogen-independent effects of progesterone on the electrophysiological excitability of dorsal midbrain neurons in golden hamsters.
复制标题
黄体酮对金黄仓鼠背侧中脑神经元电生理兴奋性的雌激素依赖性和雌激素非依赖性作用。
DOI：
10.1159/000124999
复制
发表时间：
1988
影响因子：
4.1
通讯作者：
Rose,JD
中科院分区：
文献类型：
--
作者：
Havens,MD;Rose,JD
在金仓鼠脊柱前凸反应的诱导过程中，雌二醇 (E) 和黄体酮 (P) 的联合作用被发现会导致背侧中脑神经元的活动水平、感觉反应和运动相关放电发生重大变化，而背侧中脑是该物种中脊柱前凸的重要区域。本研究调查了 E 和 P 对背侧中脑神经元的这些影响可能是通过突触兴奋性或尖峰生成过程的变化而产生的可能性。在皮下注射丙二醇媒介物中的 P 之前和之后，在切除卵巢、聚氨酯麻醉的仓鼠中，通过腹内侧中脑被盖刺激，单个背侧中脑神经元被顺向或逆向激活。 P注射产生两种神经生理学效应：（1）强烈抑制跨突触激活，（2）在逆向侵入的神经元中，体细胞树突尖峰成分的振幅发生变化（增加或减少）。这两种效应在注射 P 后迅速出现（即 10-20 分钟内）。 P 对顺向神经元兴奋性的影响取决于仓鼠的 E 启动，但相反，P 对逆向尖峰幅度的影响则不然。 P 的这些神经生理学作用的几个特征表明，该激素可能通过非基因组机制发挥作用，可能涉及神经元膜上的受体。
During the induction of lordosis responses in golden hamsters, the joint actions of estradiol (E) and progesterone (P) have been found to produce major changes in the activity levels, sensory responsiveness and movement-related firing of neurons in the dorsal midbrain, a region vital for lordosis in this species. The present study investigated the possibility that these effects of E and P on dorsal midbrain neurons might arise through changes in transsynaptic excitability or spike-generating processes. Single dorsal midbrain neurons were orthodromically or antidromically activated by ventromedial midbrain tegmental stimulation in ovariectomized, urethane-anesthetized hamsters before and after subcutaneous injection of P in propylene glycol vehicle. P injection produced two neurophysiological effects: (1) a strong depression of transsynaptic activation, and (2) in antidromically invaded neurons, a change in the amplitude (either an increase or decrease) of the soma-dendritic spike component. Both of these effects appeared rapidly (i.e. within 10–20 min) after P injection. The P effect on orthodromic neuronal excitability was contingent upon E priming of the hamsters, but, in contrast, the P effect on antidromic spike amplitude was not. Several features of these neurophysiological effects of P imply that the hormone may have been acting through nongenomic mechanisms, possibly involving receptors in neuronal membranes.