液压打击损伤后海马CA1区神经元兴奋性变化的研究

为考察脑损伤对海马CA1区锥体神经元电活动的影响并研究大黄素对神经元的超兴奋性和突触传递的作用，应用液压打击大鼠脑损伤模型和细胞外记录方法提取诱发的海马CA1区场兴奋性突触后电位(fPSP)和群峰电位(PS)，进行相关的数据处理和分析。发现损伤侧比非损伤侧的fPSP斜率明显升高，PS波峰个教显著增加，而PS潜伏期明显减小；在灌流液中施加大黄素，CA1区诱发场电位明显减弱。研究结果表明：颅脑损伤可造成海马CA1区锥体神经元的迟发性过度兴奋；大黄素对神经元的兴奋性有抑制作用，可能对颅脑损伤后的中枢神经系统具有保护功能。

STUDY ON EXCITABILITY CHANGE OF HIPPOCAMPAL CA1 NEURONS AFTER FLUID PERCUSSION INJURY

The effects of traumatic head injury on the neuronal activity in the hippocampal CA1 area and the effects of emodin on the neuronal hyperexcitability and synaptic transmission were studied. The fluid percussion brain injury rat model and extracellular recording method were used. The field excitatory postsynaptic potential and population spike evoked by stimulating Schaffer collaterals were collected from the ipsilateral (impact side) and the contralateral rat hippocampus CA1 areas in vitro. And the field potentials, including the field excitatory postsynaptic potential and the population spike were analyzed. Results showed that the slope of the field excitatory postsynaptic potential in the ipsilateral area was obviously greater than that in the contralateral area. And the number of the population spike was increased significantly while the latency of the population spike was decreased obviously. Furthermore, the evoked field potentials in hippocampus CA1 areas were decreased significantly by emodin even after the brain injury. Studies indicated that traumatic head injury may lead to hyperexcitability of hippocampal CA1 pyramidal neurons. Emodin can depress the neuronal hyperexcitability, which suggests that emodin plays an important role in protecting the central nervous system from neuronal damage after traumatic head injury.