Nicotine is known to have an enhancing effect on cognitive performance. It enhances the reorientation of attention in visuospatial tasks [19] and alters the neuronal activity responsible for increased attention and arousal [20]. Furthermore, several studies have found associations between SNPs in multiple nicotinic receptor genes and cognitive performance [21,22]. However, effects on cognitive performance at SNPs related to nicotine dependence seem peculiar given the presumed acceleration in cognitive development over recent human history. Therefore, these results suggest that if selection is shaping the genetic landscape of these genes, it may be through their effect on cognitive function in the absence of drug use. Evidence from nicotinic receptor knockout mice also supports a role for nicotinic receptors in memory and learning, as well as anxiety levels. CHRNA7 knockout mice have impaired reaction times [23] and decreased procedural learning [24], while, CHRNA6 knockout mice show that this receptor plays a role in nicotinic modulation of dopaminergic transmission, an important component of learning and memory [25]. Based on these observations, we hypothesize that at least some of the nicotinic receptors may have
