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      Models of neuromodulation for computational psychiatry : Models of neuromodulation

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          Psychiatry faces fundamental challenges: based on a syndrome-based nosology, it presently lacks clinical tests to infer on disease processes that cause symptoms of individual patients and must resort to trial-and-error treatment strategies. These challenges have fueled the recent emergence of a novel field-computational psychiatry-that strives for mathematical models of disease processes at physiological and computational (information processing) levels. This review is motivated by one particular goal of computational psychiatry: the development of 'computational assays' that can be applied to behavioral or neuroimaging data from individual patients and support differential diagnosis and guiding patient-specific treatment. Because the majority of available pharmacotherapeutic approaches in psychiatry target neuromodulatory transmitters, models that infer (patho)physiological and (patho)computational actions of different neuromodulatory transmitters are of central interest for computational psychiatry. This article reviews the (many) outstanding questions on the computational roles of neuromodulators (dopamine, acetylcholine, serotonin, and noradrenaline), outlines available evidence, and discusses promises and pitfalls in translating these findings to clinical applications. For further resources related to this article, please visit the WIREs website.

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          Most cited references 145

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          A Neural Substrate of Prediction and Reward

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            The dopamine hypothesis of schizophrenia: version III--the final common pathway.

             O. Howes,  S Kapur (2009)
            The dopamine hypothesis of schizophrenia has been one of the most enduring ideas in psychiatry. Initially, the emphasis was on a role of hyperdopaminergia in the etiology of schizophrenia (version I), but it was subsequently reconceptualized to specify subcortical hyperdopaminergia with prefrontal hypodopaminergia (version II). However, these hypotheses focused too narrowly on dopamine itself, conflated psychosis and schizophrenia, and predated advances in the genetics, molecular biology, and imaging research in schizophrenia. Since version II, there have been over 6700 articles about dopamine and schizophrenia. We selectively review these data to provide an overview of the 5 critical streams of new evidence: neurochemical imaging studies, genetic evidence, findings on environmental risk factors, research into the extended phenotype, and animal studies. We synthesize this evidence into a new dopamine hypothesis of schizophrenia-version III: the final common pathway. This hypothesis seeks to be comprehensive in providing a framework that links risk factors, including pregnancy and obstetric complications, stress and trauma, drug use, and genes, to increased presynaptic striatal dopaminergic function. It explains how a complex array of pathological, positron emission tomography, magnetic resonance imaging, and other findings, such as frontotemporal structural and functional abnormalities and cognitive impairments, may converge neurochemically to cause psychosis through aberrant salience and lead to a diagnosis of schizophrenia. The hypothesis has one major implication for treatment approaches. Current treatments are acting downstream of the critical neurotransmitter abnormality. Future drug development and research into etiopathogenesis should focus on identifying and manipulating the upstream factors that converge on the dopaminergic funnel point.
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              The expanded biology of serotonin.

              Serotonin is perhaps best known as a neurotransmitter that modulates neural activity and a wide range of neuropsychological processes, and drugs that target serotonin receptors are used widely in psychiatry and neurology. However, most serotonin is found outside the central nervous system, and virtually all of the 15 serotonin receptors are expressed outside as well as within the brain. Serotonin regulates numerous biological processes including cardiovascular function, bowel motility, ejaculatory latency, and bladder control. Additionally, new work suggests that serotonin may regulate some processes, including platelet aggregation, by receptor-independent, transglutaminase-dependent covalent linkage to cellular proteins. We review this new "expanded serotonin biology" and discuss how drugs targeting specific serotonin receptors are beginning to help treat a wide range of diseases.

                Author and article information

                Wiley Interdisciplinary Reviews: Cognitive Science
                WIREs Cogn Sci
                May 2017
                May 2017
                September 21 2016
                : 8
                : 3
                : e1420
                [1 ]Translational Neuromodeling Unit (TNU), Institute for Biomedical Engineering; University of Zurich & Swiss Federal Institute of Technology (ETH Zurich); Zurich Switzerland
                [2 ]Wellcome Trust Centre for Neuroimaging; University College London; London UK
                [3 ]Max Planck Institute for Metabolism Research; Cologne Germany
                © 2016


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