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目的探讨海人酸(KA)颞叶癫痫(EP)发作后两种GABAB受体亚单位即GBR1a和GBR2的动态变化,以了解颞叶EP发病的受体分子生物学机制。方法应用KA颞叶EP模型及原位杂交技术检测EP发作后不同时程海马各亚区的两种亚单位mRNA表达及其单个残存正常细胞mRNA表达的变化。结果KA注射侧海马结构残存正常细胞明显减少,差异有统计学意义(P<0.01)。以CA3区细胞缺失最多。随着时间的推移,致痫鼠注射侧残存正常细胞进一步减少。致痫早期,两种亚单位mRNA表达水平广泛下降,以后CA1和CA3区持续表达低下,但有表达逐渐增加的趋势;DG区则暂时性下降后很快回升。单个残存正常细胞的亚单位mRNA表达则明显增加,尤其CA3区。结论KA注射侧海马结构普遍受损,且明显重于KA注射对侧,具有明显单侧病灶的病理改变。纠正海马结构神经元缺失后,单个残存正常细胞的mRNA表达水平上调明显,此为颞叶EP的内源性自我保护机制。
Objective To investigate the dynamic changes of two GABAB receptor subtypes (GBR1a and GBR2) following the onset of temporal lobe epilepsy (EPA) in the kainate acid (KA) so as to understand the molecular mechanism of the receptor in temporal lobe EP. Methods KA temporal lobe EP model and in situ hybridization were used to detect the mRNA expression of two subunits in hippocampus and the mRNA expression of single remaining normal cells at different time points after EP onset. Results The residual normal cells in the hippocampus of KA injection group were significantly decreased (P <0.01). To CA3 cell loss most. Over time, residual normal cells on the injected side of the epileptogenic rat were further reduced. In the early stage of epilepsy, the expressions of two subunit mRNAs decreased in a wide range. Afterwards, the expression of CA1 and CA3 remained low, but the expression gradually increased. However, DG decreased rapidly and then recovered rapidly. The expression of subunit mRNA of single remaining normal cells was significantly increased, especially in CA3 region. Conclusion The structure of hippocampus in KA injection side is generally impaired, which is obviously heavier than that of KA injection. It has obvious pathological changes of unilateral lesions. Correct the absence of hippocampal neurons, the mRNA level of single residual normal cells was significantly up-regulated, which is the endogenous self-protection mechanism of temporal lobe EP.