title: [Neurobiology of obsessive-compulsive disorder].
abstract: In the last few decades, neurobiological research has considerably improved the understanding of the pathophysiological basis of obsessive-compulsive disorder (OCD), indirectly contributing to the improvement of diverse therapy strategies. A number of functional imaging studies have indicated functional deficits in frontostriatal networks, which can be subsumed in an orbitofrontal model of obsessive-compulsive disorder. A dysfunction is postulated in parallel frontostriatal circuits, leading to an imbalance in direct and indirect feedback loops and a disinhibition of thalamocortical activity. Neurochemical studies have shown that OCD is linked to changes of the central modulatory transmitter system, especially, the serotonin and dopamine system, which probably contribute to a direct and indirect dysregulation in various neural networks. Pharmacologically, the elucidation of these serotonergic and dopaminergic alterations and their interactions are of special interest.
authors.affiliation: Klinik für Psychiatrie und Psychotherapie der, Ludwig-Maximilians-Universität, München, Deutschland.
authors.forename: S
authors.initials: S
authors.lastname: Karch
authors.forename: O
authors.initials: O
authors.lastname: Pogarell
mesh_terms: D000339:Affect / Q000502:physiology; D001364:Awareness / Q000502:physiology; D001479:Basal Ganglia / Q000503:physiopathology; D001931:Brain Mapping; D003342:Corpus Striatum / Q000503:physiopathology; D004298:Dopamine / Q000502:physiology; D005625:Frontal Lobe / Q000503:physiopathology; D006179:Gyrus Cinguli / Q000503:physiopathology; D006801:Humans; D009415:Nerve Net / Q000503:physiopathology; D009433:Neural Inhibition / Q000502:physiology; D009771:Obsessive-Compulsive Disorder / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D012701:Serotonin / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology; D013788:Thalamus / Q000503:physiopathology
chemical_list: D012701:Serotonin; D004298:Dopamine