Cocaine is one of the oldest and most widely abused stimulants in the United States, and addiction affects all income groups, ages, and ethnicities.
In 2014, there were an estimated 1.5 million cocaine users aged 12 or older (0.6 percent of the population). Adults aged 18 to 25 years have a higher rate of current cocaine use than any other age group, with 1.4 percent of young adults reporting past-month cocaine use.
Repeated cocaine use can lead to addiction. In 2014, about 913,000 Americans met the criteria for dependence or abuse of cocaine during the past 12 months.
Reports indicate that cocaine was involved in 505,224 of the nearly 1.3 million visits to emergency departments for drug misuse or abuse, which translates to over one in three drug misuse or abuse-related emergency department visits (40 percent) that involved cocaine.
There is no single cause of addiction. In some cases, addiction is related to the ingredients in the addictive substance causing chemical reactions in the body.
In other cases, addiction is partly genetic. Scientists have long known that cocaine directly stimulates the brain’s reward center and induces long-term changes to the reward circuitry that are responsible for addictive behavior.
Some of the cocaine-induced changes occur in the prefrontal cortex, which, in healthy animals, controls behaviors such as inhibitory control and emotion regulation. After cocaine abuse, changes in these structures are thought to mediate many of the symptoms that characterize addiction, such as drug-seeking, loss of control, and poor decision-making.
Alban de Kerchove d'Exaerde from the Université Libre de Bruxelles in Belgium and his colleagues uncovered a gene called Maged1 that plays a crucial role in controlling the pathological changes to the reward circuitry that are responsible for addictive behaviors.
Maged1 is a member of a family of genes active in tumors. But Maged1 also functions in the brain and may play a role in neural fating and response to antidepressants. Because activation of the Maged1 gene is altered by chronic cocaine treatment, de Kerchove d'Exaerde and colleagues investigated whether Maged1 plays a role in cocaine addiction.
The scientists observed that mice lacking the Maged1 gene were entirely unresponsive to cocaine and also that the release of dopamine in the nucleus accumbens was diminished. After more experiments with Maged1 in different brain areas, they found that it is specifically required in the prefrontal cortex and not in the neurons producing dopamine in the ventral tegmental area for the development of cocaine sensitization and dopamine release.
The findings of this study with Maged1 may be a promising step in analyzing the mechanisms underlying drug addiction and suggests the need for further investigations into the molecular mechanisms underlying addiction-associated adaptations in the brain.
