Neuroplasticity, which includes long-term potentiation (LTP), is a proposed physiological mechanism for memory formation. LTP is dependent on an optimal interaction between the glutamate (GLU), dopamine (DA) and γ-Aminobutyric acid (GABA) systems and perturbations in these systems likely explain why patients with SCZ demonstrate deficits in WM and neuroplasticity[5,6]. nAChR are present on GABA, GLU and DA neurons and nicotine could potentially improve cognition by modulating these systems. Studies have demonstrated that acute nicotine administration potentiates neural plasticity in the motor cortex of healthy human subjects. One of these studies used Paired Associative Stimulation (PAS), a powerful paradigm to index LTP in the motor cortex, to assess the effects of nicotine on LTP in non-smokers[7]. The results demonstrate that nicotine enhanced LTP-like mechanisms induced by PAS in the motor cortex[7]. To date, however, there has been no direct measure of LTP-like plasticity from the DLPFC in humans. To overcome this challenge, the investigators group has developed a novel PAS technique of combined transcranial magnetic stimulation (TMS) and electroencephalography (EEG)[8] to directly index LTP from the DLPFC.