New information about molecular mechanisms related to alcoholism and relapse may lead to new treatments for the disease.
The Study
Researchers at the University of California San Francisco conducted a study in which they provided lab rats with free access to either alcohol or sugar. After almost two months of free access, the rats were subjected to several weeks of abstinence. Those who had consumed alcohol showed increased electrical activity in the part of the brain labeled the nucleus accumbens (NAcb) core, known to play a role in motivation and goal-directed behaviors. The rats that had consumed sugar did not show an increase in electrical activity in the NAcb core during the period of abstinence. It was determined that the increased activity in the alcohol group was due to inhibition of small-conductance calcium-activated potassium (SK) channels. In the alcohol group or rats, inducing SK channel activity with drugs inhibited NAcb core activity and reduced the desire for alcohol.
What Does This Mean?
This new information indicates that a decrease in SK channel activity and an increase in NAcb core activity have an important connection to alcoholics' relapses after they quit drinking. Dr. Antonello Bonci, senior author of the study, explains the importance of this finding to the treatment of alcoholism: "Our findings are particularly exciting because the FDA-approved drug chlorzoxazone, which has been used for more than 30 years as a muscle relaxant, can activate SK channels. Although SK channels are not the only target of this drug and it can present a variety of clinical side effects, it provides an unexpected and very exciting opportunity to design human clinical trials to examine whether chlorzoxazone, or other SK activators, reduce excessive or pathological alcohol drinking."
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