This study is intended to examine the tDCS and Morris Water maze training in Alzheimer’s disease(AD) rats on Tau protein expression. Experiment groups were divided into four groups and assigned 16 rats to each group. Group Ⅰ was a control group(AD induced by scopolamine); Group Ⅱ was a experimental control group(AD injured by scopolamine and treatment tacrine); Group Ⅲ was a group of tDCS application after AD injured by scopolamine; Group Ⅳ was a group of morris water maze training after AD injured by scopolamine. In cognition test, the outcome of group Ⅱ was significantly lower than the groups(p<.001). and group Ⅲ, Ⅳ were significantly low result at 14 days(p<.05). In histological finding, the experimental groups were destroy of micro vessels and finding of cell atropy and swelling. Group Ⅲ, Ⅳ were decreased in degeneration of liver and kidney cells. In immuno- histochemistric response of BDNF and tau protein in hippocampus, BDNF expression of Group Ⅱ was more increase than the other groups. and increase of BDNF expression was Ⅲ, Ⅳ were higher than group Ⅰ at 21 days. Tau protein expression of Group Ⅱ was more decrease than the other groups. and decrease of Tau protein expression was Ⅲ, Ⅳ were lower than group Ⅰ at 21 days. These result suggest that improved tDCS and morris water maze training after scopolamine induced is associated with dynamically altered expression of BDNF and Tau protein in hippocampus and that is related with cognitive function.

This study purposed to examine the effect of low power laser on pain response and axonal regeneration. In order to prepare peripheral nerve injury models, we crushed the sciatic nerve of Sprague-Dawley rats and treated them with low power laser for 21 days. The rats were divided into 4 groups: normal group(n=10); control group(n=10) without any treatment after the induction of sciatic nerve crush injury; experimental group I(n=10) treated with low power laser(0.21mJ/㎟) after the induction of sciatic nerve crush injury; and experimental group II(n=10) treated with low power laser(5.25mJ/㎟) after the induction of sciatic nerve crush injury. We measured spontaneous pain behavior(paw withdrawal latency test) and mechanical allodynia(von Frey filament test) for evaluating pain behavioral response, and measured the sciatic function index for evaluating the functional recovery of peripheral nerve before the induction of sciatic nerve crush injury and on day 1, 7, 14 and 21 after the induction. After the experiment was completed, changes in the H & E stain and toluidine blue stain were examined histopathologically, and changes in MAG(myelin associated glycoprotein) and c-fos were examined immunohistologically. According to the results of this study, when low power laser was applied to rat models with sciatic nerve crush injury for 21 days and the results were examined through pain behavior evaluation and neurobehavioral, histopathological and immunohistological analyses, low power laser was found to affect pain response and axonal regeneration in both experimental group I and experimental group II. Moreover, the effect on pain response and axonal regeneration was more positive in experimental group I to which output 0.21mJ/㎟ was applied than in experimental group II to which 5.25mJ/㎟ was applied.

This study is intended to examine the tDCS and Montoya stair task(MST) on sensorimotor recovery and glial scar expression in MCAo induced stroke model of rat. To achieve this goal, this study selected 80 SD rats of 8 weeks. The experiment groups were divided them into four groups, and assigned 20 rats to each group. GroupⅠ was a experimental control group; GroupⅡ was a tDCS application group after MCAo; GroupⅢ was a MST application group after MCAo; GroupⅣ was a tDCS and MST application group after MCAo. In each group, neurological function test measurement, motor behavior test, montoya stair task test, immunohistochemistric finding of GFAP expression finding were analyzed. In motor behavior test, the outcome of groupⅠ was significantly difference than the other group, especially from 14days. In montoya stair task test, the outcome of groupⅠ was significantly lower than the other group especially, groupⅡ were significantly different on 14days and group Ⅳ was most significantly difference than the other group. In immunohistochemistric finding, groupⅡ, Ⅲ, Ⅳ were decrease GFAP expression on depend on time stream. These results throughout the MCAo due to focal ischemic brain injury rat model four weeks tDCS and MST was applied, when the neurobehavioural, upper extremity function and ability, histopathologic data suggest that sensorimotor function recovery and a positive influence on glial scar decrease and confirmed that.

This study is intended to examine the motor skill learning and treadmill exercise on motor performance and synaptic plasticity in the cerebellar injured rats by harmaline. Experiment groups were divided into four groups and assigned 15 rats to each group. GroupⅠ was a normal control group(induced by saline); GroupⅡ was a experimental control group(cerebellar injured by harmaline); GroupⅢ was a group of motor skill learning after cerebellar injured by harmaline; GroupⅣ was a group of treadmill exercise after cerebellar injured by harmaline. In motor performance test, the outcome of groupⅡ was significantly lower than the groupⅢ, Ⅳ(especially groupⅢ)(p<.001). In histological finding, the experimental groups were destroy of dendrities and nucleus of cerebellar neurons. GroupⅢ, Ⅳ were decreased in degeneration of cerebellar neurons(especially groupⅢ). In immunohistochemistric response of synaptophysin in cerebellar cortex, experimental groups were decreased than groupⅠ. GroupⅢ's expression of synaptophysin was more increased than groupⅡ, Ⅳ. In electron microscopy finding, the experimental groups were degenerated of Purkinje cell. These result suggest that improved motor performance by motor skill learning after harmaline induced is associated with dynamically altered expression of synaptophysin in cerebellar cortex and that is related with synaptic plasticity.