Expression Of GFAP, GLAST, GLT-1 In Gliacyte In Human Mesial Temporal Lobe Epilepsy

【Objective】To determine the expression level of glial fibrillary acidic protein (GFAP), Glutamate - cystine transporter (GLAST) and Glial glutamate transporter 1 (GLT-1) in human mesial temporal lobe epilepsy. And to find the independent factors for the neuron loss in hippocampus in human mesial temporal epilepsy.【Methods】1. Part 1 and 2: The medial temporal cortex and hippocampus from 40 patients with mesial temporal lobe epilepsy were harvested in surgery. The surgically resected hippocampus was classified into two groups. The expression and alteration of GFAP, GLAST, and GLT-1 in the specimens was assessed using immunohistochemical staining. The expression and alteration of GLASTmRNA and GLT-1mRNA in the specimen was assessed using reverse transcription polymerase chain reaction (RT-PCR). The results were observed and compared withβ-acti, quantified and compared by the Software Quantity-One.2. Part 3: A case-control study was carried out in 55 cases with temporal lobe epilepsy diagnosed by EEG ,clinic and pathological .Unvaried analysis and multivariate logistic regression analysis were performed to find the correlation between the loss of neuron in hippocampus and clinic pathological factors.【Results】1. The expression of GFAP increased in various districts of the hippocampus. A change in astrocyte morphology was observed, with astrocyte cell bodies becoming larger and processes becoming more stellate and often longer in length.2.The levels of GFAP were(55.70±26.92)(,102.52±23.55)(,34.46±8.69)(,48.01±6.24 )in total hippocampal area,CA1,CA2 and dentate gyrus in the specimens from A, respectively. Compared with group A, levels of GFAP were (26.54±7.85),(36.05±3.71),(17.03±1.87),(24.44±2.98)in the specimens from B, There were significantly difference in the two groups (P both < 0.01 ).3.The expressing of GLAST in CA1 and CA2 indicated decreases(P<0.05) from A, whereas, non-significantly change in total hippocampal area and DG compare to group B (P>0.05). the levels of GLAST were(40.50±6.02)(,45.84±7.23)(,52.67±11.51),(36.73±6.50)in total hippocampal area,CA1,CA2 and DG in the specimens from A while(41.09±5.92),(48.56±10.62),(39.39±9.48),(43.29±10.61)in group B.4.The expression of GLT-1 in the sclerotic hippocampus (CA1) decreases (P<0.05), however, the there were up regulation of them in the CA2 (P<0.05) in the specimens from A. the total expression of GLT-1 in the sclerotic hippocampus showed (150.57±28.60), with (50.57±28.60), (114.53±3.84) in CA1 and CA2 respectively; In group B, the total expression showed (178.17±61.23), with (123.40±3.58), (109.27±4.14) in CA1 and CA2 respectively.5. The expression of GLASTmRNA were (0.665±0.22),(0.703±0.16)in group A and group B respectively. There was non-significant change in the two groups.6. the expression of GLT-1mRNA were(1.025±0.18), (1.032±0.21) in group A and group B respectively. There was also non-significant change in the two groups.7. The incidence of the loss of neuron in hippocampus in temporal lobe epilepsy was 47 (85%). Single variable analysis showed that sex, familial history of epilepsy , aura, damage factor and Medication are not concerned with the loss of neuron in hippocampus, however ,age of onset (≤3 years) , course of disease(>2 years) , seizure frequency(≥1moth) , persistence time(≥60s), generalized seizure all associated with the incidence of the loss of neuron in hippocampus.8. Multivariate logistic regression analysis showed that the independent influencing factors for the loss of neuron in hippocampus in children with temporal epilepsy Included seizure frequency, persistence time and the tape of seizure.【Conclusions】1. The expression of GFAP increased in various districts of the hippocampus.2. While GLAST and GLT-1 reduction in the hippocampus CA1 area but increased in CA2 area in mesial temporal lobe epilepsy. It suggesting that the redistribution of gial glutamate transporter in hippocampus after seizures may be associated with the pathogenesis of intractable temporal lobe epilepsy.3. These data suggest that the post-transcription Modification of GLT-1mRNA and GLASTmRNA in hippocampus may be associated with the pathogenesis of intractable temporal lobe epilepsy.4. The development of the loss of neuron in hippocampus may be associated with many factors including age of onset, course of disease, seizure frequency, persistence time and generalized seizure. In order to lower the incidence of the loss of neuron, early intervening treatment is very important.