• 제목/요약/키워드: ${\theta}-burst$

검색결과 12건 처리시간 0.014초

흰쥐 해마 CA1 영역에서 H2O2에 의한 장기강화 억제에 대한 발효황금 추출물의 효과 (Effects of Fermented Scutellaria Baicalensis Extract on H2O2 - Induced Impairment of Long-term Potentiation in Hippocampal CA1 Area of Rats)

  • 허준호;;김민선
    • 동의생리병리학회지
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    • 제33권6호
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    • pp.356-362
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    • 2019
  • Scutellaria baicalensis (SB) has widely used in the treatment for various brain diseases in the field of Oriental medicine. Biofermantation of SB can make major chemical constituents of SB to pass blood-brain barrier easily and to have more potent anti-oxidant ability. There is a little information about the contribution of fermented SB (FSB) to the formation or maintenance of the neural plasticity in the hippocampus. The purpose of this study was to evaluate effects of FSB extract on hydrogen peroxide (H2O2) - induced impairments of the induction and maintenance of long-term potentiation (LTP), an electrophysiological marker for the neural plasticity in the hippocampus. From hippocampal slices of rats, the field excitatory postsynaptic potentials (fEPSPs) were evoked by the electrical stimulation to the Schaffer collaterals - commissural fibers in the CA1 areas and LTP by theta-burst stimulation by using 64 - channels in vitro multi-extracellular recording system. In order to induce oxidative stress to hippocampal slices two different concentrations (200, 400 μM) of H2O2 were given to the perfused aCSF before and after the LTP induction, respectively. The ethanol extract of FBS with concentration of 25 ㎍/ml, 50 ㎍/ml was diluted in perfused aCSF that had 200 μM H2O2, respectively. Oxidative stress by the treatment of H2O2 resulted in decrease of the induction rate of LTP in the CA1 area with a dose - dependent manner. However, the ethanol extract of FSB prevented the reduction of the induction rate of LTP caused by H2O2 - induced oxidative stress with a dose - dependent manner. These results may support a potential application of FSB to ameliorate impairments of hippocampal dependent neural plasticity or memory caused by oxidative stress.

산화질소 대사체 함유 마늘 발효 추출물 이용 혈관성 치매 흰쥐 모델의 기억력 및 신경가소성 장애 개선 효과 (Effect of Fermented Garlic Extract Containing Nitric Oxide Metabolites on Impairments of Memory and of Neural Plasticity in Rat Model of Vascular Dementia)

  • 장소영;문세진;김유지;정선오;김민선
    • 동의생리병리학회지
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    • 제36권2호
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    • pp.59-65
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    • 2022
  • Rodent model for chronic cerebral hypoperfusion caused by bilateral carotid artery occlusion (BCAO) show clinically relevant evidences for vascular dementia and impairments of synaptic plasticity in the hippocampus. The purpose of this study was to evaluate effect of fermented garlic (F-Garlic) extract with NO metabolites on cognitive behaviors, synaptic plasticity, and molecular events in the hippocampus following BCAO. Adult male Sprague-Dawley rats were randomly divided three experimental groups into: control+water; BCAO+water; BCAO+F-Garlic. Animals were treated with oral administration of F-Garlic in tap water as a drinking water after surgery for 4 weeks. On passive avoidance test and Y-maze test, BCAO+water showed a significant decrease in step-through latency and spontaneous alteration, indicating deficit of hippocampal memory formation but the treatment of F-Garlic significantly increased these cognitive behaviors. In control+water, a robust increase in the amplitude of evoked field excitatory postsynaptic potentials was observed by theta burst stimulation to hippocampal neural circuit indicating formation of long-term potentiation (LTP) in the hippocampal CA1. BCAO+water showed a highly significant deficit in LTP induction 4 weeks after BCAO. On other hand, daily oral administration of F-Garlic extract caused the marked preservation of LTP induction. Moreover, parvalbumin was markedly reduced in the CA1, especially, in the stratum radiatum of BCAO+water. In contrast, BCAO+F-Garlic mitigate a significantly reduction of the parvalbumin. In summary, these results suggest that daily oral administration of F-Garlic extract can ameliorate cognitive memory deficit through the preservation of synaptic plasticity and interneurons integrity in the hippocampus in rodent model of chronic cerebral hypoperfusion.