Background: The central role that the thalamus plays in information processing and sensory integration suggests that its dysfunction may be a factor in the pathophysiology of schizophrenia. Glutamate is a key neurotransmitter in thalamic function, and although ail aspects of thalamic glutamate neurotransmission have nor been elucidated, transcripts encoding members of each family of the glutamate receptors have been identified in rite thalamus. Recently, activation of group II metabotropic glutamate receptors (mGluRs) was demonstrated in mts to ameliorate the behavioral effects associated with exposure to phencyclidine, an uncompetitive NMDA receptor antagonist that can induce psychotic symptoms, suggesting the possibility of mGluR abnormalities in schizophrenia. We investigated whether expression of thalamic mGluR mRNA is altered in this illness. Methods: We examined the expression of the transcripts encoding the mGluR1, 2, 3, 4, 5, 7, and 8 receptors in postmortem thalamic tissue samples from elderly schizophrenic and control subjects, using in situ hybridization. We identified six thalamic nuclei in each section (anterior; dorsomedial, lateral dorsal, central medial, reticular, and nuclei of the ventral tier). Results: There were no differences between elderly schizophrenic and control subjects in the expression of mGluR1, 2, 3, 4, 5, 7, or 8 transcript levels ill any of these six thalamic nuclei. Conclusions: mGluR mRNA expression is nor abnormal in rite thalamus of patients with schizophrenia. The modulatory roles proposed for mGluRs, and the potentially important relationship between mGluRs and NMDA receptors, suggest that mGluRs may be involved in the pathophysiology of schizophrenia, blat this is not detectable at this level of gene expression. (C) 1999 Society of Biological Psychiatry.