Neither the 5-HT1A- nor the 5-HT2-Receptor Subtype Mediates the Effect of Fluvoxamine, a Selective Serotonin Reuptake Inhibitor, on Forced-Swimming-Induced Immobility in Mice

• Published in: Japanese journal of pharmacology Vol. 68; no. 1; pp. 71 - 75
• Main Authors: Egawa, Takashi, Ichimaru, Yasuyuki, Imanishi, Taiichiro, Sawa, Aiko
• Format: Journal Article
• Language: English
• Published: Kyoto The Japanese Pharmacological Society 1995; Japanese Pharmacological Society
• Subjects: Analysis of Variance; Animals; Behavior, Animal - drug effects; Biological and medical sciences; Depression model; Desipramine - pharmacology; Disease Models, Animal; Drug Interactions; Fluvoxamine; Fluvoxamine - pharmacology; Forced-swimming; Male; Medical sciences; Mice; Mice, Inbred ICR; Neuropharmacology; Pharmacology. Drug treatments; Piperazines - pharmacology; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease); Psychology. Psychoanalysis. Psychiatry; Psychopharmacology; Receptors, Serotonin - drug effects; Receptors, Serotonin - metabolism; Receptors, Serotonin, 5-HT1; Ritanserin - pharmacology; Selective serotonin reuptake inhibitor; Serotonin Antagonists - pharmacology; Forced-swimming; Fluvoxamine; Depression model; Selective serotonin reuptake inhibitor; Mood disorder; Serotoninergic receptor; Rodentia; Oral administration; Depression; Vertebrata; Chemotherapy; Mammalia; Treatment; Mouse; Animal; Antidepressant agent; Mechanism of action
• ISSN: 0021-5198; 1347-3506
• DOI: 10.1254/jjp.68.71

The effect of fluvoxamine, a selective serotonin (5-HT) reuptake inhibitor, was studied in the forced-swimming test, a model of depression, in mice. Fluvoxamine at 60 mg/kg, p.o. significantly decreased the immobility time in the forced-swimming test. A similar effect was observed by the selective norepinephrine reuptake inhibitor desipramine at the same dose. Furthermore, the suppression of immobility time was slightly potentiated by repeated administration of fluvoxamine, and a significant effect was observed at 30 mg/kg, p.o. The effect of fluvoxamine on forced-swimming was unaffected by the 5-HT2 antagonist ritanserin. On the other hand, the 5-HT1A antagonist NAN-190 (1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl] piperazine) potentiated the effect of fluvoxamine on forced-swimming. It is expected, however, that a 5-HT1A antagonist should antagonize the effect of fluvoxamine when 5-HT1A mediates the suppressive effect of fluvoxamine on the immobility time in forced-swimming. From these results, neither the 5-HT1A- nor the 5-HT2-receptor subtype is involved in the suppressive effect of fluvoxamine on the immobility associated with forced-swimming.