The neuronal activity changes by oxidative injury in OHSC using optical imaging system = The neuronal activity changes by oxidative injury in OHSC using optical imaging system

다국어 초록 (Multilingual Abstract)

Oxidative stress produces neurotoxicity often related with various CNS disorders. Ascorbic acid (AA) have been shown to have protective effects as anti-oxidants in experimental neurological disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effects of AA on kainic acid (KA) neurotoxicity using organotypic hippocampal slice cultures. AA may enhance the protection effect and benefit to improve neuronal plasticity in post-injury. Thus, we investigated that the antioxidant affects neuroprotective signaling and neuroplastic changes in hippocampus after oxidative injury. Electrophysiological and biochemical assays were used to observe changes in synaptic efficacy following electrical and/or pharmacological manipulation of synaptic function. Neuronal cell death, as assessed by propidium iodide (PI) uptake, was reduced by AA treatment compared with KA treatment. AA significantly prevented cell death and inhibited reactive oxygen species (ROS) level, and mitochondrial dysfunction. Optical imaging revealed that KA treatment tended to delay the latency of electrical stimulation and decrease the amplitude of optical signals of synaptic activity. These results suggest that AA may protect hippocampal neurons against oxidative stress and the survived neurons may functional to synaptic plasticity changes. This work was supported by the Basic Science Research Program through NRF of Korea, which is funded by the MEST (2016R1D1A3B02008194) and the Ministry of Science, ICT, and Future Planning (2014R1A2A2A04004407).