Alterations of glutamatergic neurotransmission have been postulated based upon the schizophrenia-like effects induced by phencyclidine (PCP). PCP is a potent antagonist of the NMDA receptor, a ligand gated ion channel essential for normal glutamatergic neurotransmission. Synaptic glutamate activates the NMDA receptor and is then rapidly cleared from the synapse by a family of plasma membrane EAATs. One fate of recovered glutamate is conversion to glutamine, which may subsequently be transported back to the presynaptic neuron, reconverted to glutamate, and packaged into vesicles by a vesicular glutamate transporter (vGLUT). The enzymes and transporters that comprise this so-called glutamate/glutamine cycle are candidates for dysregulation in glutamatergic synapses that may function improperly in psychiatric illness. This project utilizes in situ hybridization and western blot analysis to measure expression of EAAT1-4 in anterior cingulate, dorsolateral PFC, and several thalamic nuclei in subjects with schizophrenia and a control group. I am also leading a project examining expression of EAAT interacting proteins in this cohort using the same methodology.