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"Ativan produced significantly larger reductions in activity in the thalamus (a brain region involved with sleep regulation) than alcohol did," Volkow said. "We believe that this difference accounts for the fact that Ativan was more sedating than alcohol. Moreover, after Ativan, the reduction in thalamic activity was associated with more intense self-reports of 'sedation' and 'sleepiness.' The larger decrements in thalamic activity associated with Ativan likely reflect the fact that there are differences in sensitivity between the different types of GABA receptors to the effects of alcohol than to those of benzodiazepines. Alternatively," she added, "this could reflect the effects of alcohol on other neurotransmitters that antagonize the decrements in thalamic activity."

Alcohol induced larger decrements in the basal ganglia, which is a brain region that receives extensive innervation (supply) from dopamine, a neurotransmitter implicated in the reinforcing effects of drugs of abuse, including those of alcohol. Alcohol was perceived as more stimulating and more reinforcing than Ativan, as assessed by self-reports of 'stimulated,' 'high' and 'drug liking.'

"We know that alcohol's effects on the brain go beyond its effects on GABA receptors," said Wang. "Alcohol is a 'dirty drug' in that it acts on many brain systems, including dopamine. The larger changes in the basal ganglia caused by alcohol than by Ativan could reflect the effects of alcohol on dopamine, which in turn could account for it being perceived as more reinforcing and stimulating than Ativan."

"This study looks at a basic science question," said de Wit, " how does alcohol act on the brain? Alcohol seems to have different effects, both sedative-like and stimulant-like, on the brain. Healthy volunteers who experi
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Contact: Nora D. Volkow, M.D.
volkow@bnl.gov
631-344-3335
Alcoholism: Clinical & Experimental Research
21-Jun-2000