ABSTRACT
The earliest studies that sought to examine the ability of nicotine to enhance cognitive performance were performed in rodents, and many of these experiments were predicated on the known alerting or nootropic effect of certain CNS stimulant drugs. We entered this area in 1988
and chose to study the potential cognitive-enhancing actions of nicotine in nonhuman primates with the premise that nicotine’s actions involved more complex mechanisms than a nonspecific sharpening of attention or arousal. Interest was based largely on two findings. In studying the effects of nicotine in humans 2 years earlier, Wesnes and Warburton
concluded that nicotine facilitates state-dependent learning and does not affect associative processes. Secondly, the strong relationship between the ability of the centrally acting nicotinic receptor antagonist mecamylamine to impair performance of the retention trial of an inhibitory avoidance task in rats, and its ability to inhibit the biosynthesis of acetylcholine in cortical and limbic structures was impressive.
