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热性癫痫发作是儿童常见病,能损害认知功能,而突触可塑性和再可塑性(metaplasticity)是维系大脑认知功能的重要神经基础。本文通过脑片灌流和细胞外场电位记录术研究了热性癫痫发作大鼠海马齿状回外侧支的突触可塑性和再可塑性。制作对照组和热性癫痫发作组大鼠的脑切片后,记录电极置于齿状回外侧支的外分子层获取兴奋性突触后电位。双极刺激电极根据不同需要分别安放于齿状回外侧支或门区。结果显示,大鼠海马齿状回外侧支给予100Hz的条件刺激后,对照组和热性癫痫发作大鼠海马齿状回外侧支长时程增强(long-term potentiation,LTP)的幅度均没有显著改变。而在齿状回外侧支给予10Hz的预先刺激,再施加相同的条件刺激后,对照组外侧支LTP幅度明显下降,条件刺激后1h的相对兴奋性突触后电位(field excitatory postsynaptic potentials,fEPSP)为1.10±0.26;而热性癫痫发作组则表现出明显的LTP,条件刺激后1h的相对fEPSP为1.35±0.2,与对照组比较有显著性增强(P<0.05)。在齿状回门区实施10Hz的预先逆行性刺激,再施加与前述实验相同的条件刺激后,对照组外侧支LTP幅度亦出现明显下降,条件刺激后1h的相对fEPSP为1.15±0.14;而热性癫痫发作组表现出明显的LTP,条件刺激后1h的相对fEPSP分别为1.47±0.19,与对照组比较有显著性增强(P<0.05)。以上结果表明,热性癫痫发作可以在不改变突触可塑性的情况下影响再可塑性,从而导致神经损伤,该现象提示热性癫痫发作能通过不同途径增加神经兴奋性。
Fever seizures are common in children and can impair cognitive function, whereas synaptic plasticity and metaplasticity are important neural foundations for maintaining cognitive function in the brain. In this paper, the synaptic plasticity and re-plasticity of the hippocampal dentate gyrus in the hippocampus of rats with thermal epilepsy were studied by perfusion of brain slices and extracellular field potential recording. After the brain sections of the rats in the control group and the thermal epileptic seizure group were made, the recording electrode was placed in the outer molecular layer of the lateral branch of the dentate gyrus to obtain the excitatory postsynaptic potential. Bipolar stimulation electrodes are placed in the dentate gyrus or branch according to different needs. The results showed that the amplitude of long-term potentiation (LTP) of hippocampal dentate gyrus in control group and heat-induced seizure rats was not significantly increased after 100Hz stimulation of hippocampal dentate gyrus in rats change. However, the amplitude of LTP in the lateral branch of the control group decreased significantly after pre-stimulation of 10 Hz was given to the lateral branch of the dentate gyrus and the same excitatory postsynaptic potentials (fEPSP) (1.10 ± 0.26). However, in the seizure group, the LTP was significantly higher than that of the control group (1.35 ± 0.2) (P <0.05). In the dentate gyrus, a 10 Hz pre-retrograde stimulus was applied to the dentate gyrus, and the amplitude of the LTP in the lateral branch of the control group decreased significantly after applying the same stimulation as the previous experiment. The relative fEPSP at 1 hour after stimulation was 1.15 ± 0.14. Compared with the control group, the LTP was significantly increased in the seizure group (P <0.05). The relative fEPSP at 1 h after the stimulation was 1.47 ± 0.19, respectively (P <0.05). The above results indicate that thermal seizures can affect re-plasticity without changing synaptic plasticity, leading to nerve damage, suggesting that thermal epileptic seizures increase neural excitability through different pathways.