Dopaminergic Modulation of Synaptic Transmission in Cortex and Striatum
Among the many neuromodulators used by the mammalian brain to regulate circuit function and plasticity, dopamine (DA) stands out as one of the most behaviorally powerful. Perturbations of DA signaling are implicated in the pathogenesis or exploited in the treatment of many neuropsychiatric diseases,...
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Published in | Neuron (Cambridge, Mass.) Vol. 76; no. 1; pp. 33 - 50 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
04.10.2012
Elsevier Limited |
Subjects | |
Online Access | Get full text |
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Summary: | Among the many neuromodulators used by the mammalian brain to regulate circuit function and plasticity, dopamine (DA) stands out as one of the most behaviorally powerful. Perturbations of DA signaling are implicated in the pathogenesis or exploited in the treatment of many neuropsychiatric diseases, including Parkinson’s disease (PD), addiction, schizophrenia, obsessive compulsive disorder, and Tourette’s syndrome. Although the precise mechanisms employed by DA to exert its control over behavior are not fully understood, DA is known to regulate many electrical and biochemical aspects of neuronal function including excitability, synaptic transmission, integration and plasticity, protein trafficking, and gene transcription. In this Review, we discuss the actions of DA on ionic and synaptic signaling in neurons of the prefrontal cortex and striatum, brain areas in which dopaminergic dysfunction is thought to be central to disease.
Dopamine (DA) regulates many aspects of neuronal function. In this Review, Tritsch and Sabatini discuss the actions of DA on neuronal signaling in the prefrontal cortex and striatum, brain areas in which dopaminergic dysfunction is thought to be central to disease. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-2 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 0896-6273 1097-4199 |
DOI: | 10.1016/j.neuron.2012.09.023 |