The effect of electrical stimulation of the cerebellar fastigial nucleus on learning, memory and the expression of growth-associated protein-43 after cerebral infarction / 中华物理医学与康复杂志

ABSTRACT

Objective To study the effect of electrical stimulation of the fastigial nucleus of the cerebellum (FNS) on learning,memory and the expression of growth-association protein-43 (GAP-43) after cerebral ischemia and reperfusion.Methods Sixty healthy,adult,male Sprague-Dawley rats were randomly divided into a normal group,a sham-operation group (sham group),a model group and an FNS group,with 15 rats in each.Left middle cerebral artery occlusion and reperfusion (MCAO/R) was administered to the rats in the FNS and model groups using the thread embolism method.The rats of the FNS group were given FNS treatment using a pair of needle electrodes inserted into the cerebellar fastigial nucleus 3hrs after the MCAO/R.Needle electrodes were similarly inserted in the model group rats,but no electrical stimulus was applied.Then the rats' learning and memory abilities were tested using a Morris water maze on days 1,3 and 7 after the MCAO/R modeling.The expression of GAP-43 mRNA on the side of the cerebral infarction was detected using a quantitative,real-time polymerase chain reaction.Results The average escape]atencies of the rats in the model and FNS groups were significantly longer than those of the normal and sham groups at all time points,but the FNS group rats demonstrated a significantly shorter average escape latency than the rats of the model group at each time point.The normal and sham groups showed a significantly lower expression of GAP-43 mRNA than the model and FNS group rats at all time points.The FNS group rats had a significantly higher level of GAP-43 mRNA than the rats of the model group.Conclusion FNS improved the rats' learning and memory abilities.This might be associated with the up-regulation of GAP-43 mRNA in neurons on the side of the cerebral infarction which could promote the regeneration and repair of peripheral nerve axons in the area of the infarction.