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首页> 外文期刊>Journal of Neurophysiology >17beta-estradiol enhances NMDA receptor-mediated EPSPs and long-term potentiation.
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17beta-estradiol enhances NMDA receptor-mediated EPSPs and long-term potentiation.

机译：17β-雌二醇可增强NMDA受体介导的EPSP和长期增效作用。

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摘要

Gonadal steroid hormones influence CNS functioning through a variety of different mechanisms. To test the hypothesis that estrogen modulates synaptic plasticity in the hippocampus, in vitro hippocampal slices from 2-mo-old Sprague-Dawley male rats were used to determine the effect of 17beta-estradiol on both N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potentials (EPSPs) through intracellular recordings and long-term potentiation (LTP) through extracellular recordings. Intracellular EPSPs and extracellular field EPSPs (fEPSPs) were recorded from CA1 pyramidal cells by stimulating Schaffer collateral fibers. In intracellular experiments, slices were perfused with medium containing bicuculline (5 microM) and low Mg2+ (0.1 mM) to enhance the NMDA receptor-mediated currents and 6, 7-dinitroquinoxaline-2,3-dione (DNQX) (10 microM) to block the alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprianate (AMPA) receptor-mediated component. The effects of 17beta-estradiol on NMDA receptor-mediated activity were excitatory; concentrations >10 nM induced seizure activity, and lower concentrations (1 nM) markedly increased the amplitude of NMDA-mediated EPSPs (both the first and second responses increased during paired pulse stimulation by 180 and 197%, respectively). In extracellular experiments, slices perfused with 17beta-estradiol (100 pM) exhibited a pronounced, persisting, and significant enhancement of LTP of both the fEPSP slope (192%) and fEPSP amplitude (177%) compared with control slices (fEPSP slope = 155%; fEPSP amplitude = 156%) 30 min after high-frequency stimulation. These data demonstrate that estrogen enhances NMDA receptor-mediated currents and promotes an enhancement of LTP magnitude.
机译：性腺甾体激素通过多种不同机制影响中枢神经系统功能。为了检验雌激素调节海马突触可塑性的假设，使用了来自2个月大的Sprague-Dawley雄性大鼠的体外海马切片来确定17β-雌二醇对两种N-甲基-D-天冬氨酸（NMDA）的影响受体介导的兴奋性突触后电位（EPSPs）通过细胞内记录和长期增强（LTP）通过细胞外记录。通过刺激Schaffer侧支纤维，从CA1锥体细胞记录了细胞内EPSP和细胞外场EPSP（fEPSP）。在细胞内实验中，向切片中灌注含小分子（5 microM）和低Mg2 +（0.1 mM）的培养基以增强NMDA受体介导的电流，并向6，7-二硝基喹喔啉-2,3-二酮（DNQX）（10 microM）阻断α-氨基-3-羟基-5-甲基-4-异恶唑丙酸酯（AMPA）受体介导的成分。 17β-雌二醇对NMDA受体介导的活性具有兴奋作用。浓度> 10 nM的诱导的癫痫发作活性，而较低的浓度（1 nM）则显着增加NMDA介导的EPSP的幅度（在配对脉冲刺激过程中，第一和第二反应分别增加了180和197％）。在细胞外实验中，与对照切片相比，灌注17β-雌二醇（100 pM）的切片与对照切片相比，fEPSP斜率（192％）和fEPSP振幅（177％）的LTP显着，持续存在并且显着增强（fEPSP斜率= 155） ％; fEPSP振幅= 156％）高频刺激后30分钟。这些数据表明，雌激素增强了NMDA受体介导的电流并促进了LTP幅度的增强。

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