Previously, we have reported alterations in thalamic NMDA receptor subunit and excitatory amino acid transporter expression in schizophrenia, consistent with the hypothesis that thalamic glutamatergic dysfunction may contribute to the pathophysiology of this illness. We have generalized this hypothesis to include other molecules of the glutamate synapse. Using riboprobes specific for human brain-specific Na+-dependent inorganic phosphate transporter (BNPi) and differentiation-associated Na+/Pi co-transporter (DNPi), both vesicular glutamate transporters, in situ hybridization was performed in the thalami of persons with schizophrenia and comparison subjects. We detected increased expression of DNPi mRNA in the thalamus in schizophrenia, while BNPi mRNA was not expressed in the thalamus in any subjects. These findings support the hypothesis of glutamatergic dysfunction in the thalamus in schizophrenia. © 2001 Lippincott Williams & Wilkins.