Patients with SCZ display an unusually high prevalence of smoking and high rates of smoking cessation failures are commonly associated with WM deficits[3]. The central nicotinic acetylcholine receptor (nAChR) is the main target for nicotine. Several lines of evidence strongly suggest that the nAChR system is a promising target for treating cognitive deficits in SCZ. These include the following observations: (1) expression of nAChRs receptors is abnormal in several brain regions, including the PFC, in post mortem brains of patients with SCZ, (2) genes coding for nAChR subunits are candidate risk genes for SCZ and nicotine addiction, and (3) smoking abstinence produce deficits of WM, which correlate with blood levels of nicotine, are alleviated by smoking re-instatement and are blocked by nAChR antagonists in patients with SCZ, but not in healthy control smokers (e.g.,[4]). However, the underlying mechanism through which nicotine and nAChRs affect DLPFC-dependent memory in SCZ are still unknown. Nicotine-induced increases in neural plasticity may represent one such mechanism.