| The aim of this study is to survey gene expression profiles in nonlesional refractory temporal lobe epi lepsy (TLE) , to further verify the difference of gene expression, then to evaluate the possible molecular pathogenesis of this kind of epilepsy and can help to supply a new way for diagnosis and therapy. In the first part, the difference of gene expression was studied in 2 cases of TLE samples and 1 mixed sample from normal control tissue by methods of cDNA microarray consisting of 18000 genes. The results showed that, those different expressed genes in two TLE samples altered with the same tendency including: immune correlative genes, ionic channel transportation genes, signal conduction genes, mitochondral function genes and so on. Gene took part in all the phases during occurrence and progress of TLE, it was quite a complex procedure. In the second part, on the basis of prophase results , KCNJ4 mRNA level was tried to be examined in the temporal lobe tissue in 12 TLE patients and 10 trauma controls by RT-PCR. Compared with trauma controls, KCNJ4 mRNA level of TLE patients decreased statistically ( P<0.05 ). In the third parts, immunohistochemistry and western blotting were used to detect the changes of kir2.3 channel protein in TLE patients and controls. The results showed that, kir2.3 protein level of TLE patients also decreased statistically (P<0.05), compared with controls. From the researches of all above parts, we concluded that the change of KCNJ4 mRNA level and the decreased level of kir2. 3 channel protein in TLE patients could result in disturbing the stability of neuronal cell membrane as well as reducing the amortization ability to super-potassium loading of glial cell, affecting the maintenance of cell excitability equilibrium and finally cause epileptiform discharging. Furthermore, we evaluate that potassium channel kir2.3 subunit could be appropriate role site for those antiepileptic drugs.
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