Schizophrenia, a chronic psychiatric disorder, affects 24 million people and causes working memory deficits. Working memory is proposed to emerge from synchronized neural activity at γ-frequencies, creating transient γ-oscillations in the primary visual cortex (V1) and sustained γ-oscillations in the prefrontal cortex (PFC). These oscillations emerge from a microcircuit created by excitatory pyramidal neurons and inhibitory parvalbumin-expressing interneurons (PVI). Schizophrenic patients show a deficit of PV firing at gamma frequencies in these regions, which correlates to working memory deficits. Our preliminary computational data found different levels of excitatory drive to PVIs create distinct types of γ-oscillations. This study proposes that different levels of excitatory drive to PVIs are required to generate different types of γ-oscillations in different regions. This involves both expansion and confocal microscopy of control postmortem human brain tissues to measure the synaptic and subsynaptic level of excitatory drive to PVIs in PFC and V1. The results are expected to show a greater amount of excitatory input in the V1 region compared to the PFC, thus resulting in transient γ-oscillations in V1 and sustained γ-oscillations in PFC. This aims to understand the neural mechanisms of working memory in control patients to ultimately provide insights for future therapeutic approaches of schizophrenia.