Conventional methods of applying PAS involves the repetitive delivery of two paired stimulations: the first being an electrical peripheral nerve stimulation of the right median nerve of the hand and 25 ms later a second TMS pulse delivered to the contralateral motor cortex (hence PAS-25). Through repetitive pairing of these two stimulations, PAS-25 results in increased activation of output neurons that represents a direct measure LTP in humans[9]. The investigators lab has recently recorded PAS-LTP in the DLFPC using a novel technique of TMS-EEG[8]. Here, PAS is applied to the DLPFC by repetitive delivery of: (1) a peripheral nerve stimulation to the right side, followed 25 ms later by; (2) a TMS pulse delivered to the left DLPFC. PAS-induced potentiation of cortical evoked activity is then measured directly from the DLPFC and represents LTP in this region as interneurons activated from cortical stimulation and peripheral stimulation, in turn, activate DLPFC output neurons contemporaneously and increase their activity when repeated over 30 min. Thus, the activation of the somatosensory cortex by peripheral nerve stimulation will propagate to the DLPFC and arrive there simultaneously with the TMS pulse resulting in LTP. The validity of this technique relies on the observation that there are strong correlations between TMS induced evoked potentials in the motor and DLPFC (r=0.8-0.85, p<0.001)[8]. LTP is quantified as change in DLPFC cortical evoked activity from baseline (pre-PAS) to different time points following PAS-25 (post-PAS). Preliminary data from the investigators ongoing study using these novel methods, demonstrate that PAS-25 induces significant LTP in the DLPFC. For example, in healthy controls cortical evoked activity in the DLPFC was facilitated by 56% post-PAS (maximal point of facilitation) while in patients with SCZ the cortical evoked activity post-PAS was only increased by 16% (Cohen's d=0.80). This is to the investigators knowledge the first time LTP has ever been demonstrated in-vivo in the DLPFC of humans and the first time that LTP deficits in the DLPFC have been reported in patients with SCZ. The aim of this proposal is now to assess whether enhanced WM by nicotine is mediated by potentiation of LTP in the DLPFC.