Effect of Panax ginseng on Latency of Passive Avoidance Response and Neuronal Damage of Hippocampus

• 영문명: Effect of Panax ginseng on Latency of Passive Avoidance Response and Neuronal Damage of Hippocampus
• 발행기관: 대한생리학회-대한약리학회
• 저자명: So-Hyun Cho Sang-Hyun Choi Jae-Won Choi Dong-Hoon Kim Kyung-Ho Shin Yeon-Sook Chun Boe-Gwun Chun
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제1권 제4호, 345~353쪽, 전체 9쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 1997.01.01

영문 초록

The effects of crude saponin (SAP) and alkaloid (ALK) fractions of Panax ginseng C.A. Meyer on the detrimental effects of electroconvulsive shock (ECS) and scopolamine on passive avoidance response (PAR) were studied in male Sprague-Dawley rats, referring their effects on the neuronal injury and plasticity of hippocampus in response to electrolytic lesion of left entorhinal cortex (ECL). The detrimental ECS effect on PAR was attenuated by pre- and post-treatments with SAP and ALK, respectively, or by pretreatment with aminoguanidine (AG), an inhibitor of diamine oxidase and NO synthase. And the detrimental scopolamine effect on PAR was also inhibited by pre-treatment with ALK or AG, and by post- treatment with SAP or ALK, respectively. On the 7th day after ECL, the brain sections stained by cresyl violet and by acetylcholinesterase (AChE) histochemistry, respectively, showed the chromatolysis and numeral decrease of neurons and the reduction of AChE reactivity in the hippocampus CA1 area and to a lesser extent, in the dentate gyrus. The neuronal cell death of the CA1 area was significantly reduced by SAP, ALK, or AG, and the reduction of AChE reactivity was significantly attenuated by SAP or ALK and to a lesser extent by AG. These results suggests that the protective effect of ginseng SAP and ALK fractions on ECS- or scopolamine-induced impairment of PAR may be ascribed in part to preservation of hippocampal neurons, particularly cholinergic neurons.

키워드

ECS Scopolamine Passive avoidance response Entorhinal cortex lesion Ginseng Aminoguanidine Cholinesterase Hippocampus