Involvement of the Endocannabinoid System in Ethanol-Induced Corticostriatal Synaptic Depression

DOI Web Site PubMed 参考文献50件
  • Cho Hyeong Seok
    Department of Pharmacology, College of Medicine, The Catholic University of Korea, Korea MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Korea
  • Jeun Seung Hyun
    Department of Pharmacology, College of Medicine, The Catholic University of Korea, Korea MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Korea
  • Li Qing-Zhong
    Department of Pharmacology, College of Medicine, The Catholic University of Korea, Korea MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Korea
  • Kim Ki Jung
    Department of Pharmacology, College of Medicine, The Catholic University of Korea, Korea MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Korea
  • Choi Se Joon
    Department of Pharmacology, College of Medicine, The Catholic University of Korea, Korea MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Korea
  • Sung Ki-Wug
    Department of Pharmacology, College of Medicine, The Catholic University of Korea, Korea MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Korea

この論文をさがす

抄録

Ethanol is a wildly abused substance that causes various problems and damage in our society. We examined the connection between the action of ethanol and the endocannabinoid system in corticostriatal synaptic transmission by recording excitatory post-synaptic currents (EPSCs). Acute treatment of ethanol (100 mM) inhibited corticostriatal EPSCs. In the presence of AM 251 (5 μM), a cannabinoid 1 (CB1)-receptor antagonist, or AM 404 (5 μM), a cannabinoid transporter inhibitor, the inhibition of corticostriatal EPSCs caused by ethanol was significantly reduced. This result suggests the possibility that the endocannabinoid system is involved in the action of ethanol. To support this result, brain slices were pre-treated with WIN 55,212-2 (1 μM), a CB1-receptor agonist, following treatment of ethanol or treated with WIN 55,212-2 alone. There was no significant difference between each other, indicating that when CB1 receptors are previously activated, the effect of ethanol is blunted. These results suggest that the activation of the endocannabinoid system is one of the possible mechanisms involved in ethanol-induced corticostriatal synaptic depression.

収録刊行物

参考文献 (50)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ