Abstract
Benzquinamide, the acetate of 2-hydroxy-3-diethylcarbamyl-9,10-dimethoxy-1,2,3,4,6,7-hexahydro-11bH-benzoquinolizine, interferes with conditioned avoidance behavior in rats and monkeys. After doses of benzquinamide that reliably disrupt avoidance behavior, concentrations of noradrenaline (NA) and serotonin (5-HT) in the brain are within normal limits, and overt sedative or parasympathetic symptoms do not occur. Moreover, benzquinamide is only mildly susceptible to antagonism by monoamine oxidase (MAO) inhibition. The high specificity of behavioral activity demonstrated by benzquinamide contrasts with the nonspecific effects of its parent alcohol : the alcohol is a potent depletor of brain NA and 5-HT, highly susceptible to reversal by an MAO inhibitor, and active in producing reserpine-like symptoms. The rapid and potent effect of benzquinamide on avoidance behavior leads to the conclusion that its avoidance-disrupting activity is mediated by a mechanism other than depletion of NA and 5-HT from the brain.
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