Analysis of experimental brain injury on long-term potentiation of hippocampal neurons of the rat

在实验性脑损伤模型大鼠左侧顶叶皮质施加中度液压冲击伤(FPI)，制备水平脑片。电刺激电压敏感染料(RH-482)染色的海马CA3区锥体神经元可引起兴奋性光信号向CA1区的传播。损伤侧海马区的兴奋性光学反应增强。细胞外电极记录到的海马锥体层的场电位在同侧海马CA1区也有增强。细胞内记录显示，FPI大鼠的长时程增强(LTP)受到抑制。在FPI大鼠中，LTD相对明显。但FPI对单个CA1神经元的电生理特性无明显影响。大黄素是一种保护大脑免受头部损伤的大黄素，它抑制了Schaffer络脉神经末梢诱发和自发释放的谷氨酸。

Horizontal brain slice preparations were obtained from experimental brain injury model rats by application of moderate fluid percussion injury (FPI) to the left parietal cortex of rat brain. Electrical stimulation of hippocampal CA3 pyramidal neurons stained by voltage-sensitive dye (RH-482) evoked the propagation of excitatory optical signals to CA1 pyramidal area. The excitatory optical response was enhanced at injured site (ipsilateral) of hippocampal formation. Field potentials of hippocampal pyramidal layer recorded by extracellular electrode was also enhanced at ipsilateral hippocampal CA1 area. Intracellular recordings revealed that long-term potentiation (LTP) was depressed in FPI rats. LTD was relatively obvious in FPI rats. However, electrophysiological properties of single CA1 neurons were not obviously altered by FPI. Emodin, (an anthraquinone derivative) which protect brain from head injury, depressed the evoked and spontaneous release of glutamate from nerve terminals of the Schaffer collaterals.