Neurodevelopmental liabilities in alcohol dependence: central serotonin and dopamine dysfunction.
Bibliographic record
Abstract
Alcoholism is a complex disorder with symptoms ranging from abuse to dependence, often comorbid with depression, antisocial personality, or anxiety. Neurodevelopmental causes of the disorder are unknown but inferences are possible from current knowledge. Neurobiological studies implicate multiple brain changes, which may be characterized as premorbid or morbid. These studies have also examined specific aspects of the alcohol dependence syndrome, including alcohol reinforcement and craving. Here, we review the evidence for vulnerability factors in alcohol dependence, with an emphasis on central serotonin (5-HT) and dopamine (DA). Serotonin dysfunction likely contributes to the development of alcoholism since studies of alcohol-preferring rodents show decreased 5-HT function on many measures. We have shown that serotonin-enhancing drugs reduce consumption and craving in mild to moderate alcoholics, yet similar studies in severely dependent individuals remain inconclusive. Studies indicate that serotonin dysfunction may contribute to the development of dependence via impaired impulse control and/or mood regulation. The mesocorticolimbic dopamine pathway represents another important pathophysiological target in alcoholism. Differences in D(2) receptor density, dopamine sensitivity, and gene expression have been linked to consumption, reinforcement, craving, and relapse. However, while DA agonists reduce self-administration in animals, we found no effect in humans with long-acting bromocriptine, a D(2) agonist. Dopamine may contribute differentially to the development of dependence via its effects on alcohol wanting, reinforcement, and reward memory. Although animal experiments show consistent roles for serotonin and dopamine in alcohol dependence, human studies are not always concordant. Such discrepancies highlight the complexity of dependence-related behaviors in humans and of identifying vulnerabilities to alcoholism.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".