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A dopaminergic deficit hypothesis of schizophrenia: the path to discovery.

Journal article
Authors Arvid Carlsson
Maria L. Carlsson
Published in Dialogues in clinical neuroscience
Volume 8
Issue 1
Pages 137-42
ISSN 1294-8322
Publication year 2006
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 137-42
Language en
Keywords Animals, Antipsychotic Agents, therapeutic use, Dopamine, deficiency, metabolism, Dopamine Agonists, therapeutic use, Dopamine Antagonists, pharmacology, Humans, Models, Neurological, Receptors, Dopamine D2, physiology, Schizophrenia, drug therapy, metabolism
Subject categories Physiology


In contrast to the conventional view of dopamine involvement in schizophrenia, which posits hyperactive dopaminergic transmission, we propose that for unknown developmental and/or biochemical reasons, a primary defect occurs in efficient, tight dopaminergic synaptic transmission, triggering feedback activation and receptor upregulation, and resulting in the well-characterized increase in dopaminergic tone. This hypothesis is driven by suggestive evidence for subpopulations of dopamine D2 receptors delivering contrasting forms of dopaminergic transmission: synaptic receptors, responsible for basic dopaminergic function and subject to effective feedback control, and poorly controlled extrasynaptic receptors partly responsible for the positive symptoms of psychosis. Since the primary defect is dopamine deficiency, we term this theory the dopaminergic deficit hypothesis of schizophrenia. It is currently informing clinical studies with novel partial dopamine antagonists (dopamine stabilizers) such as ACR16, which preferentially target extrasynaptic receptors while leaving synaptic transmission and basic dopamine function intact.

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