The Neurobiological Basis of Addiction – From Choice to Habit to Compulsion

Posted on:January 13, 2017
Last Updated: November 24, 2023
Time to read: 3 minutes

Addiction is a chronic neurological disorder that involves the limbic cortico-striatal neural networks of the brain. During chronic drug exposure, there is a progressive neurobiological adaptation that promotes a loss of control over drug-seeking behaviour. Cocaine use, for example, is initially, for many, a voluntary choice that develops into a habitual goal-directed behaviour and progresses to compulsive cocaine seeking, despite serious negative consequences to the user.

In the beginning, it is the nucleus accumbens (NA) in the ventral striatum and its functional interaction with the basolateral amygdala (BLA) that are responsible for developing voluntary cocaine-seeking behaviour. The NA plays an important role in dopamine-dependent reward circuits that turn motivation into action, while the BLA provides positive consolidation of cocaine-associated memories with environmental cues.

Continued exposure to cocaine, however, causes neurobiological adaptations in the striatum, with control over cocaine-seeking habits passing to the anterior dorsolateral striatum (aDLS). This functional shift in neural control, from habitual to compulsive drug-seeking behaviour, is greatly influenced by drug-associated Pavlovian conditioned stimuli that induce drug-cravings and even relapses after abstinence.

However, the neural mechanisms that underlie this transition to long-term, compulsive drug seeking are unclear. To answer this, researchers from the University of Cambridge and the University of Poitiers have analysed amygdala-striatal circuits in rats that were trained to seek cocaine in an attempt to understand how long-term maintenance of maladaptive cocaine-seeking habits develop.

 

References

New Circuit For Addiction

Murray et al., Basolateral and central amygdala differentially recruit and maintain dorsolateral striatum-dependent cocaine-seeking habits, Nature Communications, 6:10088, December 2015