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首页> 外文期刊>The European Journal of Neuroscience >High pressure modulation of NMDA receptor dependent excitability.
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High pressure modulation of NMDA receptor dependent excitability.

机译：NMDA受体依赖性兴奋性的高压调节。

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摘要

Pressure above 1.1 MPa induces in mammals and humans the high pressure neurological syndrome (HPNS). HPNS is characterized by cognitive and motor decrements associated with sleep disorders, EEG changes, tremor, and convulsions that ultimately may lead to death. Previous theories proposed that augmented response of the glutamatergic N-methyl-d-aspartate receptor (NMDAR) or reduced GABAergic inhibition may be involved. Recently, we have reported that isolated NMDAR response was augmented at high pressure. We now test whether this augmentation induces neuronal hyperexcitability. We studied high pressure effects on pharmacologically isolated NMDAR field excitatory postsynaptic potentials (fEPSPs) and on their efficacy in generating population spikes (PSs). Sprague-Dawley male rats were used. Hippocampal coronal brain slices were prepared, constantly superfused with physiological solutions, gas-saturated at normobaric pressure, and compressed up to 10.1 MPa with helium. fEPSPs and PSs were recorded from thedendritic and the somatic layers of CA1 pyramidal neurons in response to Schaefer collaterals stimulation with trains of five stimuli at 25 Hz. Pressure caused PSs to appear earlier in the train. However, PS delay, rise time and decay time were increased and PS amplitude, frequency, and number were decreased in the last responses in the train. The decrease in late fEPSPs was associated with a reduction of the total number of PSs in the train, apparently without a change in the synaptic efficacy. These results may partially explain the neuronal hyperexcitability observed at pressure. Therefore, it is postulated that significant hyperexcitability is attained at pressure only when the normal fast fEPSP is intact.
机译：高于1.1 MPa的压力在哺乳动物和人类中诱发高压神经系统综合症（HPNS）。 HPNS的特征是与睡眠障碍，脑电图变化，震颤和抽搐有关的认知和运动能力下降，最终可能导致死亡。先前的理论提出，可能涉及增强谷氨酸能N-甲基-d-天冬氨酸受体（NMDAR）的反应或降低GABA能抑制。最近，我们报道了孤立的NMDAR反应在高压下会增强。现在我们测试这种增强是否诱导神经元过度兴奋。我们研究了高压对药理学分离的NMDAR场兴奋性突触后电位（fEPSPs）及其在产生种群峰值（PSs）中的作用。使用Sprague-Dawley雄性大鼠。制备海马冠状脑切片，不断注入生理溶液，在常压下使气体饱和，并用氦气压缩至10.1 MPa。响应于在25 Hz下对五个刺激序列的Schaefer侧支刺激，从CA1锥体神经元的树突层和体细胞层记录了fEPSP和PS。压力导致PS在列车中出现得更早。但是，在列车的最后响应中，PS延迟，上升时间和衰减时间增加，PS振幅，频率和数量减少。晚期fEPSPs的减少与火车中PS总数的减少有关，显然突触效力没有变化。这些结果可以部分解释在压力下观察到的神经元过度兴奋。因此，假定只有正常的快速fEPSP完整时，才能在压力下获得明显的过度兴奋。

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