NMDA Receptor-dependent Inhibition of Synaptic Transmission by Acute Ethanol Treatment in Rat Corticostriatal Slices

  • Choi, Se-Joon (Department of Pharmacology, College of Medicine, The Catho University of Korea) ;
  • Kim, Ki-Jung (Department of Pharmacology, College of Medicine, The Catho University of Korea) ;
  • Choi, Hyeong-Seok (Department of Pharmacology, College of Medicine, The Catho University of Korea) ;
  • Kim, Seong-Yun (Department of Pharmacology, College of Medicine, The Catho University of Korea) ;
  • Yim, Dong-Seok (Department of Pharmacology, College of Medicine, The Catho University of Korea) ;
  • Cho, Young-Jin (Department of Pharmacology, College of Medicine, The Catho University of Korea) ;
  • Hahn, Sang-June (Department of Pharmacology, College of Medicine, The Catho University of Korea) ;
  • Sung, Ki-Wug (Department of Pharmacology, College of Medicine, The Catho University of Korea)
  • Published : 2006.12.31

Abstract

The effects of ethanol on corticostriatal synaptic transmission were examined, using extracellular recording and analysis of population spike amplitudes in rat brain slices, to study how acute ethanol intoxication impairs striatal function. Ethanol caused a decrease in population spike amplitudes in a dose dependent manner ($50{\sim}200mM$). Pretreatment with picrotoxin, a ${\gamma}-amino$ butyric acid $(GABA)_{A}$ receptor antagonist, increased the population spikes but ethanol (100 mM) was still effective in decreasing the population spikes under this condition. In the presence of $_{(DL)}-2-amino-5-phosphonovaleric$ acid (APV), N-methyl-D-aspartate (NMDA) receptor antagonist, the inhibitory action of ethanol on population spikes was not shown. These results suggest that ethanol inhibits the glutamatergic corticostriatal synaptic transmission through blockade of NMDA receptors.

Keywords

References

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