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Dopamine metabolism and receptor function after acute and chronic ethanol
Journal of Neurochemistry
|July 1, 1980
Summary
Acute ethanol exposure increases striatal dihydroxyphenylacetic acid (DOPAC) in rats. Chronic ethanol alters dopamine receptor binding and enkephalin levels, suggesting dopaminergic involvement in ethanol
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Ethanol consumption affects brain function.
- Dopaminergic pathways are implicated in substance abuse.
Purpose of the Study:
- To investigate the effects of acute and chronic ethanol treatment on striatal dopamine metabolites and receptor binding in rats.
- To explore the role of dopaminergic mechanisms in mediating central ethanol effects.
Main Methods:
- Rats were administered ethanol acutely and chronically.
- Striatal tissue was analyzed for dihydroxyphenylacetic acid (DOPAC) levels.
- Specific [3H]spiroperidol binding and met-enkephalin content were measured.
- Kinetic analysis of receptor binding was performed.
Main Results:
- Acute ethanol increased striatal DOPAC.
- Chronic ethanol did not alter striatal DOPAC levels.
- Chronic ethanol selectively increased [3H]spiroperidol binding affinity and met-enkephalin content in the striatum.
- Increased affinity, not number, of binding sites was observed.
Conclusions:
- Dopaminergic mechanisms at both pre- and postsynaptic levels are likely involved in the central effects of ethanol.
- Chronic ethanol exposure leads to adaptive changes in the dopaminergic system.