Abstract
Electrophysiological and biochemical approaches were used to assess possible changes in central 5-HT neurotransmission in mice that had been subjected to chronic ultramild stress for 8 weeks. This treatment produced a significant decrease in the potency of the 5-HT1A agonist ipsapirone to inhibit the electrical activity of serotoninergic neurons in the dorsal raphe nucleus, without modifying 5-HT1A receptor binding in various brain areas. These data demonstrate that chronic ultramild stress triggers a long term and durable functional desensitization of somatodendritic 5-HT1A autoreceptors in mice.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / physiology
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Animals
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Brain Chemistry / physiology
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Chronic Disease
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Corticosterone / metabolism
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Electrophysiology
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Hydroxyindoleacetic Acid / metabolism
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Inbred DBA
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Neurons / metabolism
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Neurons / physiology
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Pyrimidines / pharmacology
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Receptors, Serotonin / drug effects
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Receptors, Serotonin / physiology*
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Receptors, Serotonin, 5-HT1
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Serotonin / metabolism
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Serotonin / physiology
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Serotonin Receptor Agonists / pharmacology
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Stress, Psychological / physiopathology*
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Synaptic Transmission / physiology
Substances
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Pyrimidines
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Receptors, Serotonin
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Receptors, Serotonin, 5-HT1
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Serotonin Receptor Agonists
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Serotonin
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Hydroxyindoleacetic Acid
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ipsapirone
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Corticosterone