NMDA Receptor-dependent Inhibition of Synaptic Transmission by Acute Ethanol Treatment in Rat Corticostriatal Slices.
- Author:
Se Joon CHOI
1
;
Ki Jung KIM
;
Hyeong Seok CHO
;
Seong Yun KIM
;
Dong Seok YIM
;
Young Jin CHO
;
Sang June HAHN
;
Ki Wug SUNG
Author Information
1. Department of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul, Korea. sungkw@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Striatum;
Ethanol;
Extracellular recording;
Population spike;
Glutamate receptor;
Synaptic transmission
- MeSH:
Animals;
Brain;
Butyric Acid;
Ethanol*;
N-Methylaspartate*;
Picrotoxin;
Rats*;
Receptors, Glutamate;
Receptors, N-Methyl-D-Aspartate;
Synaptic Transmission*
- From:The Korean Journal of Physiology and Pharmacology
2006;10(6):303-307
- CountryRepublic of Korea
- Language:English
-
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.
