Ethanol as a neurochemical surrogate of
conventional reinforcers: the dopamine-opioid link
by
Di Chiara G, Acquas E, Tanda G
Department of Toxicology,
University of Cagliari, Italy.
Alcohol 1996 Jan-Feb; 13(1):13-7

ABSTRACT

Various lines of evidence support the view that ethanol is a neurochemical surrogate of conventional reinforcers, such as food and sex. In fact, ethanol activates central neuronal systems that utilize dopamine, opioids, and gamma-aminobutyric acid (GABA) as neurotransmitters and also are activated by conventional reinforcers. These neurotransmitter systems are likely to mediate specific aspects of ethanol's reinforcing properties. Activation of the mesolimbic dopamine and endogenous opioid systems might be the substrate of the incentive and rewarding (ergotropic) properties of ethanol (arousal, euphoria, motor stimulation) and of the process of acquiring ethanol-related secondary reinforcers (incentive learning) and ethanol self-administration habits. Stimulation of the endogenous GABAergic system might mediate the sedative and drive-reducing (trophotropic) properties of ethanol. The dopamine and opioid systems are largely interconnected. Thus, pharmacological blockade of the endogenous opioid system by mu- or delta-opioid receptor antagonists prevents ethanol's activation of the dopamine system and reduces ethanol consumption. This interaction might contribute to naltrexone's effectiveness in reducing alcohol craving in humans.

GABA
Opioids
Reward
Serotonin
Dopamine
Tianeptine
Barbiturates
Benzodiazepines
GHB and alcoholism
SSRIs and alcoholics
Alcohol and citalopram
The motivation for beer
Drug-induced cell suicide
Tryptophan and alcoholism
Nicotine-ethanol interaction
Alcohol, suicide and serotonin
Opioids, dopamine and alcohol
Alcohol, alcoholism and GABA(A) receptors

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