The cerebellum is known to control balance, equilibrium, and muscle tone. If the cerebellum becomes damaged, the body is unable to retain its balancing functions or involuntary muscle movement. This is why, in stroke patients, there is a high risk of functional disability, as well as a myriad of other disabilities secondary to stroke. Ischemia was induced in SD mice by occluding the common carotid artery for 5 minutes, after which blood was reperfused. Needle electrode electrical stimulation(NEES) was applied to acupuncture points, at 12, 24, and 48 hours post-ischemia on the joksamri. Protein expression was investigated through caspase-3 antibody immuno-reactive cells in the cerebral nerve cells and Western blotting. The results were as follows: The number of caspase-3 reactive cells in the corpus cerebellum 12 and 24 hours post-ischemia was significantly (p<.05) smaller in the NEES group compared to the GI group. caspase-3 expression 12 and 24 hours post-ischemia was significantly(p<.05) smaller in the NEES group compared to the GI group. Based on these results, NEES seems to have a significant effect on Caspase-3 in the cerebellum in an ischemic state at 12 and 24 hours post ischemia, NEES delays the occurrence of early stage apoptosis-inducing Caspase-3, delaying and inhibiting apoptosis. Further systematic studies will have to be conducted in relation to the application of this study’s results on stroke patients.

Ischemia, the leading cause of strokes, is known to be deeply related to synaptic plasticity and apoptosis in tissue damage due to ischemic conditions or trauma. The purpose of this study was to research the effects of NEES(needle electrode electrical stimulation) in brain cells of ischemiainduced rat, more specifically the effects of Poly[ADP-ribose] polymerase(PARP) on the corpus striatum. Ischemia was induced in SD mice by occluding the common carotid artery for 5 minutes, after which blood was re-perfused. NEES was applied to acupuncture points, at 12, 24, and 48 hours post-ischemia on the joksamri, and at 24 hours postischemia on the hapgok. Protein expression was investigated through PARP antibody immuno-reactive cells in the cerebral nerve cells and western blotting. The number of PARP reactive cells in the corpus striatum 24 hours post-ischemia was significantly(p<.05) smaller in the NEES group compared to the global ischemia(GI) group. PARP expression 24 hours post-ischemia was very significantly smaller in the NEES group compared to the GI group. Results show that ischemia increases PARP expression and stimulates necrosis, making it a leading cause of death of nerve cells. NEES can decrease protein expression related to cell death, protecting neurons and preventing neuronal apoptosis.