Journal of Oriental Neuropsychiatry (동의신경정신과학회지)

The Korean Society of Oriental Neuropsychiatry (대한한방신경정신과학회)
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Anticonvulsant Effects of JeongGan-Tang and Its Putative Action Mechanism

정간탕(定癎湯)의 항경련(抗痙攣) 효과(效果) 및 작용기전에 관한 연구(硏究)

  • Kong, Dae-Jong (Dept. of Oriental Neuropsychiatry, College of Oriental Medicine, Dongguk University) ;
  • Jeong, Hee-Sang (Dept. of Oriental Neuropsychiatry, College of Oriental Medicine, Dongguk University) ;
  • Lee, Dong-Ung (Dept.of Biotechnology, College of Science and Technology, Dongguk University) ;
  • Kim, Geun-Woo (Dept. of Oriental Neuropsychiatry, College of Oriental Medicine, Dongguk University) ;
  • Koo, Byung-Soo (Dept. of Oriental Neuropsychiatry, College of Oriental Medicine, Dongguk University)
  • 공대종 (동국대학교 한의과대학 신경정신과학교실) ;
  • 정희상 (동국대학교 한의과대학 신경정신과학교실) ;
  • 이동웅 (동국대학교 과학기술대학 생명공학과) ;
  • 김근우 (동국대학교 한의과대학 신경정신과학교실) ;
  • 구병수 (동국대학교 한의과대학 신경정신과학교실)
  • Published : 2007.12.30
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Abstract

This study was performed to examine the anticonvulsant effects of the extracts of JeongGan-Tang and explanation of its action mechanism. Method: 1) The inhibitory effect on convulsions induced by pentylenetetrazole, picrotoxin and strychnine was investigated in vivo 2) The inhibitory effect on GABA transaminase activity was evaluated in vivo and in vitro. 3) The brain GABA level and glutamate level in pentylenetetrazole-induced convulsion model were analyzed by HPLC, Results: 1) JeongGan-Tang showed the significant effect on the pentylenetetrazole-induced convulsion, which may mean that its anticonvulsant effect would be resulted from the activation of GABA receptor and chloride channel rather than the presynaptic- or postsynaptic inhibition. 2) JeongGan-Tang exhibited proper inhibitory activity on GABA transaminase in vitro and in vivo. 3) JeongGan-Tang increased the brain GABA level but did not affect the brain glutamate content, which may suggest that this drug supresses the convulsion by increase of GABA, an inhibitory neurotransmitter. Conclusion : JeongGan-Tang can be used as an anticonvulsant prescription by the modulation of GABAergic neurotramission.

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