Various lines of evidence support the view that ethanol is a neurochem
ical surrogate of conventional reinforcers, such as food and sex. In f
act, 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 reinforci
ng properties. Activation of the mesolimbic dopamine and endogenous op
ioid systems might be the substrate of the incentive and rewarding (er
gotropic) properties of ethanol (arousal, euphoria, motor stimulation)
and of the process of acquiring ethanol-related secondary reinforcers
(incentive learning) and ethanol self-administration habits. Stimulat
ion 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 block
ade of the endogenous opioid system by mu- or delta-opioid receptor an
tagonists prevents ethanol's activation of the dopamine system and red
uces ethanol consumption. This interaction might contribute to naltrex
one's effectiveness in reducing alcohol craving in humans.