OBJECTIVE: To explore the mechanisms of electro-acupuncture (EA) in improving synaptic plasticity after cerebral ischemic injury. METHODS: Focal cerebral ischemia (FCI) model was established by middle cerebral artery occlusion (MCAO) with heat-coagulation method. The changing rules of synaptic ultrastructure, synaptophysin (P38), growth-associated protein-43 (GAP-43), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the ischemic cortex 2 and 5 weeks after FCI and the effects of EA on them were observed. RESULTS: Expression of numerical density (Nv), surface density (Sv), volume density (Vv), post synaptic density (PSD) and P38 in the ischemic cortex significantly decreased after MCAO (P<0.01). Among them, Nv and Sv were raised at the 5th week in FCI rats either treated or untreated with EA (P<0.01), but the increment of Sv was higher in those of the treated rats (P<0.01); PSD in the EA treated rats also showed a significant increase at the 5th week, which was significant higher than that in those untreated; EA showed insignificant influence on Vv and synaptic interfacial curvature; P38 lowered continuously after 2 weeks, but at the 5th week, it was higher in EA treated rats than that in untreated rats (P<0.01), while at the 2nd week, the levels in treated and untreated rats were equal. GAP-43 rose in the 2nd week after modeling, with no difference between EA treated and untreated animals, at the 5th week, it was lowered in untreated rats to near that in sham-operated rats, but maintained at higher level in EA treated rats; NGF and BDNF positive cells significantly increased after modeling (P<0.01), and showed a descending trend with the time going (P<0.01) both in rats treated or untreated with EA. CONCLUSION: EA can protect synaptic ultrastructure, promote the expression of P38, GAP-43, NGF and BDNF in the ischemic cerebral cortex, and thus improve synaptic plasticity in cerebral ischemic rats.
OBJECTIVE: To explore the mechanisms of electro-acupuncture (EA) in improving synaptic plasticity after cerebral ischemic injury. METHODS: Focal cerebral ischemia (FCI) model was established by middle cerebral artery occlusion (MCAO) with heat-coagulation method. The changing rules of synaptic ultrastructure, synaptophysin (P38), growth-associated protein-43 (GAP-43), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the ischemic cortex 2 and 5 weeks after FCI and the effects of EA on them were observed. RESULTS: Expression of numerical density (Nv), surface density (Sv), volume density (Vv), post synaptic density (PSD) and P38 in the ischemic cortex significantly decreased after MCAO (P<0.01). Among them, Nv and Sv were raised at the 5th week in FCIrats either treated or untreated with EA (P<0.01), but the increment of Sv was higher in those of the treated rats (P<0.01); PSD in the EA treated rats also showed a significant increase at the 5th week, which was significant higher than that in those untreated; EA showed insignificant influence on Vv and synaptic interfacial curvature; P38 lowered continuously after 2 weeks, but at the 5th week, it was higher in EA treated rats than that in untreated rats (P<0.01), while at the 2nd week, the levels in treated and untreated rats were equal. GAP-43 rose in the 2nd week after modeling, with no difference between EA treated and untreated animals, at the 5th week, it was lowered in untreated rats to near that in sham-operated rats, but maintained at higher level in EA treated rats; NGF and BDNF positive cells significantly increased after modeling (P<0.01), and showed a descending trend with the time going (P<0.01) both in rats treated or untreated with EA. CONCLUSION: EA can protect synaptic ultrastructure, promote the expression of P38, GAP-43, NGF and BDNF in the ischemic cerebral cortex, and thus improve synaptic plasticity in cerebral ischemicrats.