However, there were significant differences in brain activity changes induced by these two drugs, she noted. 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. Alcohol was perceived as more stimulating and more reinforcing than Ativan, as assessed by self-reports of stimulated, high and drug liking.
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. These individuals may be abusing alcohol or benzodiazepines as a means to automedicate an anxiety disorder. In addition, one could speculate that chronic alcohol administration could result in decreases in brain GABA activity that could make an individual vulnerable to the sedative effects of alcohol. Back to the top. . . Platelet Adenylyl Cyclase Activity as a Trait Marker of Alcohol Dependence.