Enhanced Dopamine Transporter Density in Psychotropic-Naive Patients With Obsessive-Compulsive Disorder Shown by [¹²³I]β-CIT SPECT

Abstract

The results of our study provide direct evidence for an involvement of the dopaminergic system in the pathophysiology of OCD.

The Role of the Striatum in Compulsive Behavior in Intact and Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System

“…Experiment 2 showed that the OFC lesion-induced increase in compulsive lever-pressing can be blocked by intrastriatal administration of the SSRI paroxetine. The OFC lesions in this study are similar to those in our previous reports (Joel et al, 2005a, b), and are confined mainly to the lateral, ventrolateral, and ventral orbital regions, according to the terminology of Van de Werd and Uylings (2008). The striatal region targeted in Experiment 2, as well as in Experiments 3 and 4, is a ventromedial region of the dorsal striatum (ie, of the caudate-putamen) that is innervated by the ventral and ventrolateral orbital regions (Schilman et al, 2008), as well as by the dorsal part of the prelimbic cortex, whose terminal field extends also more dorsally in the striatum, and to a much lesser extent by the ventral prelimbic cortex (Berendse et al, 1992).…”

“…There is, however, little direct evidence for abnormalities of striatal dopamine and/or serotonin in OCD. One such piece of evidence comes from recent reports of increased density of the dopamine transporter in the striatum of OCD patients (Kim et al, 2003;van der Wee et al, 2004). Although several studies have assessed the density of the serotonergic transporter in OCD patients, none reported changes in this protein in the striatum (for review see Goddard et al, 2008).…”

Association analysis between a VNTR intron 8 polymorphism of the dopamine transporter gene (SLC6A3) and obsessive- compulsive disorder in a Brazilian sample

“…For instance, neuroimaging studies have revealed abnormalities in brain regions densely endowed with dopaminergic terminals, such as the basal ganglia. In some studies, Dopamine D2 receptor binding potential is decreased 9 and dopamine transporter binding potential is up-regulated in the basal ganglia of OCD patients which is compatible with the hypothesis of an enhanced dopaminergic activity 10 . In addition, dopamine releasing agents and uptake inhibitors, such as metilfenidate, cocaine, bromocriptine, and bupoprion, exacerbate obsessive-compulsive symptoms (OCS) in OCD patients 11 .…”

Alpha activity in the insula accompanies the urge to neutralize in sub-clinical obsessive-compulsive participants

“…This progression seems comparable to the pattern of addiction, in which a drug is initially taken freely in order to experience its rewarding effects, but eventually is considered essential, the rewarding effects decrease, and the individual feels it necessary to take ever increasing amounts (Denys, 2011). This model is supported by neurobiological similarities between OCD and addiction disorders, such as increased dopamine overactivity in ascending pathways involving D2/3 receptors Hesse et al, 2005;Van der Wee et al, 2004;Volkow & Fowler, 2000;Volkov et al, 1993Volkov et al, , 2001) and defective processing of natural rewards (Figee et al, 2011;Nielen, den Boer & Smid, 2009). The similarity of OCD and addictive circuitry is also shown in a review by Van den Heuvel et al (2010), who illustrates that a similar disinhibition of ventral and inhibition of dorsal fronto-striatal pathways is present in cocaine dependency and impulse control in Parkinson's disease as is present in OCD.…”