Korean J Physiol Pharmacol.  2006 Dec;10(6):303-307.

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

Affiliations
  • 1Department of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul, Korea. sungkw@catholic.ac.kr
  • 2Department of Physiology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
  • 3MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.

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 (50~200 mM). 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.

Keyword

Striatum; Ethanol; Extracellular recording; Population spike; Glutamate receptor; Synaptic transmission

MeSH Terms

Animals
Brain
Butyric Acid
Ethanol*
N-Methylaspartate*
Picrotoxin
Rats*
Receptors, Glutamate
Receptors, N-Methyl-D-Aspartate
Synaptic Transmission*
Butyric Acid
Ethanol
N-Methylaspartate
Picrotoxin
Receptors, Glutamate
Receptors, N-Methyl-D-Aspartate
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