Abstract
Abstract Olfactory bulb ablation in the rat produces an acquisition deficit in a step-down passive avoidance test, hyper-reactivity to environmental stimuli, elevated plasma-11-hydroxycorticosterone, and a deficit in the thermoregulatory response to low ambient temperatures, which is not evident at normal ambient temperatures. Like the other features of the bulbectomy syndrome, this thermoregulatory deficit is not related to anosmia per se, since rats made peripherally anosmic with intranasal ZnSO4 (5%) do not show a thermoregulatory deficit at low ambient temperatures. The abnormal response to cold could be prevented by chronic daily administration of amitriptyline (10mg kg−1), mianserin (10mg kg−1), and the 5-HT uptake inhibitor, Org 6582 (10 mg kg−1) for 7 days. The possibility that the thermoregulatory deficit has the same biochemical basis as the behavioural changes is discussed and a 5-HT involvement in the syndrome is considered.
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