Clearly, nicotine can enhance cognitive function and propagate LTP and thereby these processes are likely, at least in part, what underlie the highly addictive nature of this compound. Reports from human users of cognitive deficits and strong cue-induced cravings during nicotine withdrawal undoubtedly contribute to the high incidence of relapse. Medications that target neural substrates directly involved in both learning and addiction may offer a novel pharmacotherapeutic approach for nicotine dependence as well as other drugs of abuse. More intriguing yet is the possibility that novel therapeutic avenues may be directed to diminish drug-associated memories or facilitate the formation of new memories with less maladaptive behavioral consequences.
