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Korean Red Ginseng Extract Activates Non-NMDA Glutamate and GABAA Receptors on the Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis in Mice
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  • Korean Red Ginseng Extract Activates Non-NMDA Glutamate and GABAA Receptors on the Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis in Mice
  • Korean Red Ginseng Extract Activates Non-NMDA Glutamate and GABAA Receptors on the Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis in Mice
저자명
Yin. Hua,Park. Seon-Ah,Park. Soo-Joung,Han. Seong-Kyu
간행물명
Journal of ginseng research
권/호정보
2011년|35권 2호|pp.219-225 (7 pages)
발행정보
고려인삼학회
파일정보
정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Korean red ginseng (KRG) is a valuable and important traditional medicine in East Asian countries and is currently used extensively for botanical products in the world. KRG has both stimulatory and inhibitory effects on the central nervous system (CNS) suggesting its complicated action mechanisms. The substantia gelatinosa (SG) neurons of the trigeminal subnucleus caudalis (Vc) are involved in orofacial nociceptive processing. Some studies reported that KRG has antinociceptive effects, but there are few reports of the functional studies of KRG on the SG neurons of the Vc. In this study, a whole cell patch clamp study was performed to examine the action mechanism of a KRG extract on the SG neurons of the Vc from juvenile mice. KRG induced short-lived and repeatable inward currents on all the SG neurons tested in the high chloride pipette solution. The KRG-induced inward currents were concentration dependent and were maintained in the presence of tetrodotoxin, a voltage gated $Na^+$ channel blocker. The KRG-induced inward currents were suppressed by 6-cyano-7-nitroquinoxaline-2,3-dione, a non-N-methyl-D-aspartate (NMDA) glutamate receptor antagonist and/or picrotoxin, a gamma-aminobutyric acid $(GABA)_A$ receptor antagonist. However, the inward currents were not suppressed by d,l-2-amino-5-phosphonopentanoic acid, an NMDA receptor antagonist. These results show that KRG has excitatory effects on the SG neurons of the Vc via the activation of non-NMDA glutamate receptor as well as an inhibitory effect by activation of the $GABA_A$ receptor, indicating the KRG has both stimulatory and inhibitory effects on the CNS. In addition, KRG may be a potential target for modulating orofacial pain processing.