Abstract
Significant interest in the mechanistic underpinnings of obsessive-compulsive disorder (OCD) has fueled research on the neural origins of compulsive behaviors. Converging clinical and preclinical evidence suggests that abnormal repetitive behaviors are driven by dysfunction in cortico-striatal-thalamic-cortical (CSTC) circuits. These findings suggest that compulsive behaviors arise, in part, from aberrant communication between lateral orbitofrontal cortex (OFC) and dorsal striatum. An important body of work focused on the role of this network in OCD has been instrumental to progress in the field. Disease models focused primarily on these regions, however, fail to capture an important aspect of the disorder: affective dysregulation. High levels of anxiety are extremely prevalent in OCD, as is comorbidity with major depressive disorder. Furthermore, deficits in processing rewards and abnormalities in processing emotional stimuli are suggestive of aberrant encoding of affective information. Accordingly, OCD can be partially characterized as a disease in which behavioral selection is corrupted by exaggerated or dysregulated emotional states. This suggests that the networks producing OCD symptoms likely expand beyond traditional lateral OFC and dorsal striatum circuit models, and highlights the need to cast a wider net in our investigation of the circuits involved in generating and sustaining OCD symptoms. Here, we address the emerging role of medial OFC, amygdala, and ventral tegmental area projections to the ventral striatum (VS) in OCD pathophysiology. The VS receives strong innervation from these affect and reward processing regions, and is therefore poised to integrate information crucial to the generation of compulsive behaviors. Though it complements functions of dorsal striatum and lateral OFC, this corticolimbic-VS network is less commonly explored as a potential source of the pathology underlying OCD. In this review, we discuss this network’s potential role as a locus of OCD pathology and effective treatment.
Highlights
Francisco, USA Eric Burguière, Centre National de Recherche Scientifique, France Mazen A
These findings suggest that compulsive behaviors arise, in part, from aberrant communication between lateral orbitofrontal cortex (OFC) and dorsal striatum
This suggests that the networks producing obsessive-compulsive disorder (OCD) symptoms likely expand beyond traditional lateral OFC and dorsal striatum circuit models, and highlights the need to cast a wider net in our investigation of the circuits involved in generating and sustaining OCD symptoms
Summary
Though the DSM-5 classifies OCD and related disorders as a separate entity, based on potential unique neurobiological substrates, it was originally categorized as an anxiety disorder in older versions of the DSM (Stein et al, 2010; American Psychiatric Association D-TF, 2013). Different symptom clusters may be produced by different neuronal or circuit abnormalities, and future work should address how the data and ideas covered here can be applied to different subtypes of OCD; (3) We focus on VS circuitry, with the understanding that other brain regions, including dorsal striatum, are clearly important to the pathophysiology of OCD, and that circuits including dorsal and VS are likely to be cooperative, and not antagonistic (Insel and Winslow, 1992; Graybiel and Rauch, 2000; Milad and Rauch, 2012; Burguière et al, 2013, 2015; Gremel and Costa, 2013; Gillan and Robbins, 2014; Pauls et al, 2014) Despite these caveats, investigating corticolimbic-VS circuitry and developing more expansive OCD models that take limbic information processing into account (Milad and Rauch, 2012; de Haan et al, 2013; Ahmari and Dougherty, 2015) are likely to help elucidate the pathophysiologic processes leading to OCD
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