Abstract
Compulsivity has been recently characterized as a manifestation of an imbalance between the brain׳s goal-directed and habit-learning systems. Habits are perhaps the most fundamental building block of animal learning, and it is therefore unsurprising that there are multiple ways in which the development and execution of habits can be promoted/discouraged. Delineating these neurocognitive routes may be critical to understanding if and how habits contribute to the many faces of compulsivity observed across a range of psychiatric disorders. In this review, we distinguish the contribution of excessive stimulus-response habit learning from that of deficient goal-directed control over action and response inhibition, and discuss the role of stress and anxiety as likely contributors to the transition from goal-directed action to habit. To this end, behavioural, pharmacological, neurobiological and clinical evidence are synthesised and a hypothesis is formulated to capture how habits fit into a model of compulsivity as a trans-diagnostic psychiatric trait.
Highlights
Evidence from studies employing a range of techniques including lesions (Corbit and Balleine, 2003; Yin et al, 2004; Faure et al, 2005) and optogenetics (Gremel and Costa, 2013) in rodents to functional (Valentin et al, 2007; de Wit et al, 2009; Tricomi et al, 2009; Liljeholm et al, 2015) and structural imaging in humans have converged on the importance of the caudate nucleus and medial orbitofrontal cortex (OFC) for goal-directed control over action and the putamen for the gradual build-up of stimulus-response habit links over time
Different drugs of abuse vary in their pharmacological mechanisms of action, and have differential direct effects on habit learning and goaldirected control, here we focus on their shared rewarding properties which, much like any primary reinforcer, stamp in stimulus-response habitual associations over time
The finding that aberrant caudate hyperactivity was associated with urges to perform habits in our task adds weight to the suggestion that excessive habits in this disorder are most likely a consequence of failures in goal-directed control over action. This notion converges with the broader suggestion that compulsivity as a trans-diagnostic trait may be characterized by abnormalities in goal-directed structures and that this may be separable from the direct effects of drug/food rewards on stimulus-response habit-learning in the putamen
Summary
Our brains are equipped with a so-called ‘goaldirected’ system that exerts control over habits in light of new information, including changes in the desirability of outcomes (e.g. not seeking food when satiated) and changes to the contingency between actions and outcomes (e.g. when we need to turn a key in the opposite direction to what is typical to unlock a door) The balance between these systems is susceptible to disruption by a range of factors, of which several have been well characterized: those include over-training (Adams, 1982), stress (Schwabe and Wolf, 2009), associative learning conflict (de Wit et al, 2009), working memory demands (Otto et al, 2013a), and the correlation between actions and consequent outcomes (Dickinson et al, 1983). We will discuss the possible implications of these ideas for a future of individually tailored treatment assignment
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