Journal
TRENDS IN NEUROSCIENCES
Volume 30, Issue 8, Pages 399-406Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2007.06.006
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Funding
- NIAAA NIH HHS [R37 AA008459, P50 AA006420, P60 AA006420-24, AA08459, P60 AA006420, R01 AA008459, AA06420, R01 AA008459-17] Funding Source: Medline
- NIDDK NIH HHS [P01 DK026741, P01 DK026741-280004, DK26741] Funding Source: Medline
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Recent data indicate that alcohol dependence induces long-term neuroadaptations that recruit a negative emotional state. This leads to excessive alcohol ingestion motivated by relief of negative emotionality. A key mechanism in this transition to negative reinforcement is a recruitment of corticotropin-releasing factor (CRF) signaling within the amygdala. Long term upregulation, of CRF, receptors is observed in the amygdala following a history of dependence, and CRF antagonists selectively block emotionality, excessive alcohol drinking and stress-induced reinstatement of alcohol-seeking in post-dependent animals. Innate upregulation of CRF, receptor expression mimics the post-dependent phenotype, both with regard to emotional responses and ethanol self-administration. Therefore, the CRF system is emerging as a key element of the neuroadaptive changes driving alcoholism and as a major target for its treatment.
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