Abstract
Serotonin [5-hydroxytryptamine (5-HT)] neurotransmission in the central nervous system modulates depression and anxiety-related behaviors in humans and rodents, but the responsible downstream receptors remain poorly understood. We demonstrate that global disruption of 5-HT2A receptor (5HT2AR) signaling in mice reduces inhibition in conflict anxiety paradigms without affecting fear-conditioned and depression-related behaviors. Selective restoration of 5HT2AR signaling to the cortex normalized conflict anxiety behaviors. These findings indicate a specific role for cortical 5HT2AR function in the modulation of conflict anxiety, consistent with models of cortical, "top-down" influences on risk assessment.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anxiety / physiopathology*
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Cerebral Cortex / metabolism*
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Conditioning, Psychological
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Conflict, Psychological
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Depression / physiopathology
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Exploratory Behavior
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Fear
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Limbic System / metabolism
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Mice
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Mice, Knockout
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Patch-Clamp Techniques
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Periaqueductal Gray / metabolism
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Prosencephalon / metabolism
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Receptor, Serotonin, 5-HT2A / genetics
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Receptor, Serotonin, 5-HT2A / metabolism*
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Receptor, Serotonin, 5-HT2C / metabolism
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Receptors, Neurotransmitter / metabolism
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Risk-Taking
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Serotonin / physiology
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Signal Transduction*
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Synaptic Transmission
Substances
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Receptor, Serotonin, 5-HT2A
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Receptor, Serotonin, 5-HT2C
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Receptors, Neurotransmitter
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Serotonin