Abstract
Deficits in social interaction are hallmarks of neurological and psychiatric disorders. However, its underlying mechanism is still unclear. Here, we show that the loss of dendritic cell factor 1 (Dcf1) in the nervous system of mice induces social interaction deficiency, autism-like behaviour, and influences social interaction via the dopamine system. Dopamine receptor D1 agonist rescues this social cognition phenotype, and improves short-term plasticity. Together, this study presents a new genetic mechanism that affects social interaction and may provide a new way to improve positive social interaction and treat autism spectrum disorders.
Keywords:
DA; DRD1; Dcf1; Social interaction.
Copyright © 2017 Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / administration & dosage
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Animals
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Dopamine / administration & dosage
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Dopamine / metabolism
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Dopamine Agonists / administration & dosage
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Excitatory Postsynaptic Potentials
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Hippocampus / drug effects
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Hippocampus / metabolism
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Hippocampus / physiology
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Interpersonal Relations*
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Male
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Membrane Proteins / genetics
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Membrane Proteins / physiology*
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Mice, Inbred C57BL
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Mice, Knockout
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / physiology*
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Neuronal Plasticity
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Receptors, Dopamine D1 / metabolism
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Receptors, Dopamine D1 / physiology*
Substances
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Dopamine Agonists
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Membrane Proteins
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Nerve Tissue Proteins
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Receptors, Dopamine D1
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Tmem59 protein, mouse
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2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine
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Dopamine