Abstract
Methylazoxymethanol (MAM)-induced cortical hypoplasia resulted in a 20% decrease in the Bmax of 5-HT2A receptors in the frontal cortex with no change in the Bmax of 5-HT1A receptors. Chronic treatment with amitriptyline did not further decrease the Bmax of 5-HT2A receptors in the MAM-lesioned cortex, suggesting that the persistent down-regulation of cortical 5-HT2A receptors in MAM-lesioned rats was induced by serotonergic hyperinnervation.
Copyright 1998 Elsevier Science B.V.
MeSH terms
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8-Hydroxy-2-(di-n-propylamino)tetralin / pharmacology
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Alkylating Agents*
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Amitriptyline / pharmacology*
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Animals
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Antidepressive Agents, Tricyclic / pharmacology*
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Behavior, Animal / drug effects
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Cerebral Cortex / drug effects
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Cerebral Cortex / metabolism
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Female
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Ketanserin / metabolism
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Ketanserin / pharmacology
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Kinetics
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Male
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Methylazoxymethanol Acetate / analogs & derivatives*
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Microcephaly / chemically induced
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Microcephaly / metabolism*
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Pregnancy
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Rats
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Rats, Wistar
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Receptors, Serotonin / drug effects*
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Serotonin Antagonists / pharmacology
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Serotonin Receptor Agonists / pharmacology
Substances
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Alkylating Agents
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Antidepressive Agents, Tricyclic
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Receptors, Serotonin
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Serotonin Antagonists
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Serotonin Receptor Agonists
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Amitriptyline
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Methylazoxymethanol Acetate
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8-Hydroxy-2-(di-n-propylamino)tetralin
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Ketanserin
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methylazoxymethanol