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Ischemia, theleadingcauseofstrokes, isknowntobedeeplyrelatedtosynapticplasticityandapoptosisintissuedamageduetoischemicconditionsortrau-ma(1). Therearetwokindsofcelldeath: necrosisandapoptosis. Necrosisisapassivedeaththatoccursinthecentralregionofbraindamagefollowingischemia. Poly(ADP-ribose) polymerase(PARP) isactivatedwhenvariousenzymeswithinthecellnucleuscausedamagetoDNA, resultinginnecro-sis(2, 3). Italsoplaysaroleincelldifferentiationandgeneticexpression(4). PARPconservesDNAthroughaprocessinwhichADP-riboseispassedontohis-tonesandvariousothernucleonicproteins, includingitself(5). PARPusesNAD+ asasupplierofADP-ribose(6), andcelldeathoccurswhenPARPisover-activated, andATPandNAD+ areoverused, result-inginlossofenergy(7, 8, 9, 10, 11, 12).Continuousischemicconditionsinthebraincauselackofcollateralcirculation, resultingintheentirebrainsufferingacutecerebralinfarctandahighmortalityrate(13). Thiskindofpermanentdamagedoesnotoccuriftheischemiaistemporary(5-10minutes), andisfollowedimmediatelybyreperfu-sion; however, delayedneuronaldeath–lossofneu-ronsinspecificareassuchasthehippocampusorbasalgangliahasbeenobserved3-4 dayspostischemia(13, 14).Thepositiveeffectsofanorientalmedicineapproachinthetreatmentofdiseaseshavealreadybeenestablished. Orientalmedicineusesacombina-tionofpharmaceuticals,puncturetherapy,andphys-icalmethods(15).Thetreatmenteffectsofelectro-puncturevaryaccordingtostimuliconditions–thewavepatternandlengthofstimulationaffectacti-vationofserotoninneurons(16). Unlikeotherpunc-turemethods, electropuncturehastheadvantageofcontinuousstimulationaswellasallowingforobjec-tiveadjustmentoftheamountofstimulation given,making it an even more effective tool in the treat-ment of debilitating illnesses such as neural pain orparalysis(15).This study applied NEES to the joksamri and hapgok

Effects of NEES on PARP Expression in the Corpus Striatum in Rats Induced with Transient Global Ischemia