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CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model
Donna L Gruol1, Khanh Vo1, Jennifer G Bray1
1Molecular and Cellular Neuroscience Department, The Scripps Research Institute La Jolla, CA, USA.
Frontiers in Integrative Neuroscience
|April 29, 2014
Summary
Chronic ethanol exposure alters brain function by increasing CCL2, a chemokine. This study found that elevated CCL2 levels interact with ethanol, affecting synaptic proteins in the hippocampus without toxicity.
Area of Science:
- Neuroscience
- Neuroimmunology
- Molecular Biology
Background:
- Chronic ethanol exposure causes behavioral deficits linked to neuroadaptive changes.
- Ethanol induces glial cells to produce elevated levels of the chemokine CCL2, which can persist after exposure.
- CCL2-ethanol interactions may mediate ethanol's effects on the brain, particularly in the hippocampus.
Purpose of the Study:
- To investigate the interaction between CCL2 and ethanol on hippocampal synaptic function.
- To examine these interactions in a transgenic mouse model with elevated glial CCL2 expression, mimicking conditions in alcoholics.
Main Methods:
- Utilized two chronic ethanol exposure paradigms: voluntary drinking and combined drinking with vapor exposure (to induce dependence).
- Assessed effects on hippocampal synaptic proteins in CCL2 transgenic mice versus non-transgenic controls.
Main Results:
- Both ethanol exposure paradigms showed modest effects on hippocampal synaptic protein levels in CCL2 transgenic mice.
- These findings suggest an interaction between ethanol and CCL2 at the synaptic level.
- No toxic effects of CCL2 or CCL2-ethanol interactions were observed.
Conclusions:
- Ethanol-induced astrocyte production of CCL2 contributes to neuroadaptive changes.
- These changes interact with ethanol's direct actions, influencing brain function.
- The study supports a role for neuroimmune factors in the neurobiology of alcohol effects.
