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首页> 外文期刊>Brain research >Estrogen attenuates neuronal excitability in the insular cortex following middle cerebral artery occlusion.
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Estrogen attenuates neuronal excitability in the insular cortex following middle cerebral artery occlusion.

机译：雌激素减弱大脑中动脉闭塞后岛状皮层神经元的兴奋性。

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The current investigation examined the role of estrogen in the insular cortex (IC) under both normal and ischemic conditions. Experiments were done in anaesthetized male Sprague-Dawley rats. The effect of systemic 17beta-estradiol (estrogen) administration on levels of amino acids and of endogenous estrogen obtained by microdialysis and its effect on neuronal activity of cells located in the insular cortex were measured in the absence of, and following permanent occlusion of, the right middle cerebral artery (MCA). In normal rats, intravenous (i.v.) injection of estrogen resulted in a significant increase (greater than 25 spikes/bin) in the spontaneous activity of neurons located within the insular cortex, while there was a significant decrease in gamma-aminobutyric acid (GABA) levels measured in IC dialysate. Middle cerebral artery occlusion (MCAO) resulted in a biphasic response consisting of a transient increase in the extracellular concentration of glutamate, aspartate, and GABA, followed by sustained elevations in glutamate and aspartate, but reduced GABA levels 4 h post-MCAO. MCAO also resulted in a significant increase in neuronal activity in the IC (from 28+/-9 to 120+/-88 spikes/bin). This MCAO-induced excitation was completely blocked following the prior intravenous administration of estrogen. Systemic estrogen administration also resulted in a delay in the progression and decrease in the final infarct volume by approximately 56%. Taken together, these results suggest that under normal conditions, estrogen excites neurons in the insular cortex by decreasing GABA release (disinhibition) and it plays a role in attenuating the MCAO-induced excitability and death of these neurons.
机译：当前的研究检查了在正常和缺血情况下雌激素在岛状皮层（IC）中的作用。实验是在麻醉的雄性Sprague-Dawley大鼠中进行的。在不存在或永久性闭塞的情况下，测定了全身性17β-雌二醇（雌激素）对通过微透析获得的氨基酸和内源性雌激素水平的影响及其对岛状皮层细胞神经元活性的影响。右大脑中动脉（MCA）。在正常大鼠中，静脉内（iv）注射雌激素会导致岛状皮层内神经元的自发活动显着增加（大于25个峰值/箱），而γ-氨基丁酸（GABA）显着减少IC透析液中测量的水平。大脑中动脉闭塞（MCAO）导致双相反应，包括谷氨酸，天冬氨酸和GABA的细胞外浓度的瞬时增加，随后谷氨酸和天冬氨酸的持续升高，但MCAO后4小时GABA含量降低。 MCAO还导致IC中神经元活动的显着增加（从28 +/- 9增至120 +/- 88峰值/箱）。在事先静脉内注射雌激素后，这种MCAO诱导的兴奋作用被完全阻断。全身性雌激素给药还导致进展延迟和最终梗塞体积减少约56％。综上所述，这些结果表明，在正常情况下，雌激素通过减少GABA的释放（抑制作用）来激发小岛皮层中的神经元，并在减弱MCAO诱导的这些神经元的兴奋性和死亡中发挥作用。

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