Abstract
The olfactory bulbectomized (OB) rat has been developed as an animal model of depression. In the novel ‘open field’ environment, OB rats showed a hyperactivity which was attenuated by chronic treatment with desipramine (7·5 mg/kg) for 20 days. Neutrophil phagocytosis was suppressed by the lesion, which was reversed by desipramine administration. Results from serum ‘crossover’ studies and enzyme assay showed that a factor is present in the serum, and cellular enzymes are altered in the OB rat, which may be responsible for abnormal neutrophil phagocytosis. After bulbectomy, the concentrations of noradrenaline (NA) and dopamine (DA) were decreased, and the 5-hydroxyindole-3-acetic acid (5-HIAA) was increased in the brain limbic system of OB rats. Desipramine treatment significantly increased the concentration of NA and DA, and slightly decreased the 5-HIAA. These results suggest that the change in the neutrophil function following bulbectomy is similar to that reported in the depressed patient. Thus desipramine is an effective antidepressant for reversing lesion-induced changes in neurotransmitter, behaviour and neutrophil phagocytosis. © 1997 by John Wiley & Sons, Ltd.
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