Effect of chronic amitriptyline administration on serotonergic receptors in rats with methylazoxymethanol-induced microencephaly

Methylazoxymethanol (MAM)-induced cortical hypoplasia resulted in a 20% decrease in the B max of 5-HT 2A receptors in the frontal cortex with no change in the B max of 5-HT 1A receptors. Chronic treatment with amitriptyline did not further decrease the B max of 5-HT 2A receptors in the MAM-lesioned...

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Veröffentlicht in:	Brain research 1998-03, Vol.787 (2), p.333-336
Hauptverfasser:	Watanabe, Masayuki, Kodama, Yoshio, Hagino, Yoko, Nonaka, Ryo-ichi, Kaichi, Yasusuke
Format:	Artikel
Sprache:	eng
Schlagworte:	5-HT 1A receptor 5-HT 2A receptor 8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology Alkylating Agents Amitriptyline - pharmacology Animals Antidepressant Antidepressive Agents, Tricyclic - pharmacology Behavior, Animal - drug effects Biological and medical sciences Cerebral Cortex - drug effects Cerebral Cortex - metabolism Female Ketanserin - metabolism Ketanserin - pharmacology Kinetics Male Medical sciences Methylazoxymethanol Methylazoxymethanol Acetate - analogs & derivatives Microcephaly - chemically induced Microcephaly - metabolism Microencephaly Neuropharmacology Pharmacology. Drug treatments Pregnancy Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopharmacology Rats Rats, Wistar Receptors, Serotonin - drug effects Serotonin Antagonists - pharmacology Serotonin Receptor Agonists - pharmacology Wet-dog shake
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Zusammenfassung:	Methylazoxymethanol (MAM)-induced cortical hypoplasia resulted in a 20% decrease in the B max of 5-HT 2A receptors in the frontal cortex with no change in the B max of 5-HT 1A receptors. Chronic treatment with amitriptyline did not further decrease the B max of 5-HT 2A receptors in the MAM-lesioned cortex, suggesting that the persistent down-regulation of cortical 5-HT 2A receptors in MAM-lesioned rats was induced by serotonergic hyperinnervation.
ISSN:	0006-8993 1872-6240
DOI:	10.1016/S0006-8993(97)01489-3