OBJECTIVE: To explore the postsynaptic density (PSD) proteins related with the development of temporal lobe epilepsy (TLE). METHODS: Five SD rats were injected intra-peritoneally with lithium chloride and then pilocarpine twice to establish epilepsy models. At last 24 rats developed TLE, and 12 developed non-TLE. Then rats underwent intraperitoneal injection of normal saline (Norm group). Thirty days after the appearance of epilepticus the rats were decapitated with their brains taken out. The PSD proteins were extracted and purified by using sucrose gradient centrifugation and membrane sequence extraction, isolated by using two-dimensional gel electrophoresis. PDQuest software was used to screen the specifically and differentially expressed protein spots. Partial differentially expressed PSD protein spots were selected and identified by MALDI-TOF-MS. Several identified proteins were detected in the PSD fraction by Western blotting. RESULTS: Compared with the non-TLE and Norm groups, there were 40 differential protein spots in the TLE group. The expression levels of heat shock protein-27 (HSP-27), fructose-bisphosphate aldolase A (FBA), creatine kinase (CK), thyroid receptor-interacting protein 6 (TRIP6), myelin basic protein S (MBP), and LIM domain were up-regulated, but the expression levels of tubulin, actin, internexin-alpha, peptidyl-prolyl cis-trans isomerase (PPIase), sorting nexin 3 (SNX3), aconitate hydratase (ACO), glyceradehydea-3-phosphate dehydrogenase (GADPH), and succinate-coenzyme A ligase (SCOAL) were down-regulated in the TLE group. The HSP27, tubulin-alpha, and SNX3 were in the PSD gels were immunostaining positive in the 3 groups. CONCLUSION: The differential expression of PSD proteins in TLE may be due to injury induced neural plasticity. But the degree thereof may contribute to the development of TLE. These identified proteins can be regarded as important candidates for or against the development of TLE.
OBJECTIVE: To explore the postsynaptic density (PSD) proteins related with the development of temporal lobe epilepsy (TLE). METHODS: Five SD rats were injected intra-peritoneally with lithium chloride and then pilocarpine twice to establish epilepsy models. At last 24 rats developed TLE, and 12 developed non-TLE. Then rats underwent intraperitoneal injection of normal saline (Norm group). Thirty days after the appearance of epilepticus the rats were decapitated with their brains taken out. The PSD proteins were extracted and purified by using sucrose gradient centrifugation and membrane sequence extraction, isolated by using two-dimensional gel electrophoresis. PDQuest software was used to screen the specifically and differentially expressed protein spots. Partial differentially expressed PSD protein spots were selected and identified by MALDI-TOF-MS. Several identified proteins were detected in the PSD fraction by Western blotting. RESULTS: Compared with the non-TLE and Norm groups, there were 40 differential protein spots in the TLE group. The expression levels of heat shock protein-27 (HSP-27), fructose-bisphosphate aldolase A (FBA), creatine kinase (CK), thyroid receptor-interacting protein 6 (TRIP6), myelin basic protein S (MBP), and LIM domain were up-regulated, but the expression levels of tubulin, actin, internexin-alpha, peptidyl-prolyl cis-trans isomerase (PPIase), sorting nexin 3 (SNX3), aconitate hydratase (ACO), glyceradehydea-3-phosphate dehydrogenase (GADPH), and succinate-coenzyme A ligase (SCOAL) were down-regulated in the TLE group. The HSP27, tubulin-alpha, and SNX3 were in the PSD gels were immunostaining positive in the 3 groups. CONCLUSION: The differential expression of PSD proteins in TLE may be due to injury induced neural plasticity. But the degree thereof may contribute to the development of TLE. These identified proteins can be regarded as important candidates for or against the development of TLE.