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.

A stroke is the major cause of death and can cause neurological damage. The striatum serves as an input gate of the basal ganglia in assisting motor behavior. The activity-dependent synaptic plasticity in the dorsal striatum (DS) is known to play a key role for recovery of motor control after brain injury. Exercise supports functional recovery from ischemic brain injury through brain-derived neurotrophic factor (BDNF) -induced synaptic plasticity. Exercise upregulate the levels of BDNF within both the hippocampus and cerebral cortes and might act as a gate that primes the brain to respond to environmental stimulation, while simultaneously increasing the ability of neurons to resist insult. However, little is known about the effects of exercise on neuroprotection in the DS. Therefore, in this study we attempted to investigate the effects of exercise on the neuronal cell population in the DS. Transient focal brain ischemia was induced by middle cerebral artery occlusion (MCAO) on male Sprague-Dawley rats (300±30). Animals were subjected to forced treadmill exercise group and sedentary group after MCAO. Exercise improved neurologic functions measured by modified neurological severity score. Exercise group showed reduced infarct volume measured by vital staining with 2,3,5-triphenyltetrazolium chloride. Immunohistochemical analysis was performed in the DS with antibodies of neuronal nuclei (NeuN) protein, glial fibrillary acidic protein (GFAP), a matured neuronal marker and an astrocyte marker respectively and BDNF. Ischemic injury decreased NeuN+ cell population but exercise attenuated this decrease while increase in GFAP+ cell population induced by MCAO was inhibited by exercise. These findings suggest that the neurological function recovery by exercise after ischemic brain injury may be mediated by alteration of neuronal cell population in the DS.