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Escalating ethanol intake is associated with altered corticostriatal BDNF expression
Marian L Logrip1, Patricia H Janak, Dorit Ron
1The Gallo Research Center, University of California, San Francisco, Emeryville, California 94608, USA.
Journal of Neurochemistry
|May 21, 2009
Summary
Chronic alcohol exposure disrupts brain-derived neurotrophic factor (BDNF) signaling in the brain, impairing protective mechanisms against alcohol-related behaviors. This disruption persists even after abstinence, contributing to addiction
Area of Science:
- Neuroscience
- Addiction Research
- Molecular Biology
Background:
- Alcoholism is characterized by persistent neuronal adaptations and relapse, even after abstinence.
- Brain-derived neurotrophic factor (BDNF) in the dorsal striatum mediates a protective mechanism against alcohol's effects.
- Acute alcohol exposure increases BDNF, reducing sensitivity to alcohol-related behaviors.
Purpose of the Study:
- To investigate the impact of chronic ethanol exposure on the BDNF-mediated protective mechanism.
- To determine if prolonged alcohol access dysregulates BDNF signaling and increases ethanol intake.
- To assess the recovery of BDNF function after a period of abstinence.
Main Methods:
- Rodent model of chronic ethanol access (6 weeks).
- Measurement of BDNF mRNA and protein levels in the dorsal striatum and cortex.
- Assessment of ethanol-induced behavioral sensitivity and intake.
- Evaluation of BDNF levels after a 2-week abstinence period.
Main Results:
- A single ethanol bout increased dorsal striatal BDNF mRNA, but this effect was lost after 6 weeks of daily ethanol access.
- Chronic ethanol consumption decreased cortical BDNF levels, a key source for the striatum.
- These alterations in BDNF signaling persisted after 2 weeks of abstinence, indicating a lack of recovery.
Conclusions:
- The BDNF pathway's protective function against alcohol effects breaks down with chronic ethanol exposure.
- Altered BDNF signaling in the dorsal striatum and cortex may contribute to the inflexibility of addictive behaviors.
- The lack of BDNF recovery after abstinence suggests a potential target for addiction treatment.
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