Tryptamine impairs the acquisition of a one-way active avoidance task.

The effects of intraperitoneal administration of tryptamine to rats pretreated with iproniazid, on the acquisition of an unsignalled one-way active avoidance task, were examined. Tryptamine at 2.5 and 5 mg/kg significantly increased the number of trials required to perform this task to a 9/10 consecutive avoidances criterion, without affecting escape performance. The iproniazid pretreatment had no affect on acquisition, or any other performance variable, of the task. Tryptamine did not significantly affect the avoidance response, or escape response latencies; further tryptamine did not alter gross locomotor activity measured as photocell counts. These results suggest that the acquisition deficit was not the result of nonassociative effects such as changes in response capability, general activity level or nociception. The acquisition deficit induced by tryptamine may involve a direct stimulation of central 5-HT receptors since it was not induced by systemically administered 5-HT, was reversed by the 5-HT antagonists methysergide and metergoline, but was not affected by depletion of brain 5-HT, with PCPA, or by the dopamine antagonist haloperidol. Possible behavioural mechanisms for the action of tryptamine are discussed.