No evidence for selective GABAergic interneuron deficits in the anterior thalamic complex of patients with schizophrenia.

Fewer neurons have been reported in the anterior thalamic complex (AT) of individuals diagnosed with schizophrenia in comparison to control tissue. In addition, the density of presumptive thalamo-cortical relay neurons of the AT is reported to be significantly decreased in schizophrenia compared with controls whilst total AT neuron density appears unchanged. We have investigated whether schizophrenia alters either the density of presumptive interneurons or the ratio between the two fundamental neuron types within the AT by immunohistochemically visualizing GABAergic neurons in post-mortem brain tissue from individuals with a diagnosis of schizophrenia pair-matched to tissue from normal individuals. Qualitative observations indicated no obvious differences between the two cohorts in the morphology of neurons exhibiting a GABAergic phenotype. A cell counting analysis of AT neurons revealed: (1) a non-significant 1% increase in density of GABAergic neurons in schizophrenia compared with controls and (2), a non-significant 6% increase in the percentage of neurons with a GABAergic phenotype in the schizophrenia group compared with controls. These findings suggest that a reduction of AT neuron number in schizophrenia does not alter either the morphology of neurons with a GABAergic phenotype or the ratio of neuronal phenotypes within AT.