NEITHER THE 5-HT1A-RECEPTOR NOR THE 5-HT2-RECEPTOR SUBTYPE MEDIATES THE EFFECT OF FLUVOXAMINE, A SELECTIVE SEROTONIN REUPTAKE INHIBITOR, ON FORCED-SWIMMING-INDUCED IMMOBILITY IN MICE

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.