Abstract
Previous studies have indicated that ethanol (EtOH) has a relatively specific effect on excitatory synaptic transmission by inhibiting function of the N-methyl-d-aspartate receptor. We have found that EtOH potently inhibits N-methyl-d-aspartate-mediated synaptic currents in the basolateral amygdala, a brain region associated with actions of anxiolytic agents such as EtOH. This inhibitory effect of EtOH requires the presence of magnesium (Mg++). The dependence of the effect of EtOH on the presence of Mg++ suggests a possible molecular site of the action of EtOH in the vicinity of Mg++ binding sites on the N-methyl-d-aspartate receptor-channel complex. Because EtOH consumption may result in reductions in free brain Mg++, this dynamic interaction between EtOH and Mg++ may have important implications for understanding the behavioral effects of EtOH.
Footnotes
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Send reprint requests to: Dr. Scott D. Moore, Room 25, Bldg 16, Durham VA Medical Center, Durham, NC 27705.
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↵1 This work was supported by VA Merit Review and NIAAA R 29 AA 10994-01.
- Abbreviations:
- EtOH
- ethanol
- Mg++
- magnesium
- NMDA
- N-methyl-d-aspartate
- ACSF
- artificial cerebrospinal fluid
- BMI
- bicuculline methiodide
- DNQX
- 6,7 dinitroquinoxaline
- HEPES
- 4-(2-hydroxyethyl)-piperazineethanesulfonic acid
- BAPTA
- 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’,-tetraacetic acid
- APV
- d,1-2-amino-5-phosphonovaleric acid
- GABA
- γ-aminobutyric acid
- EPSP
- excitatory postsynaptic potential
- EPSC
- excitatory postsynaptic current
- Received March 12, 1998.
- Accepted June 1, 1998.
- The American Society for Pharmacology and Experimental Therapeutics
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