Our transcriptomic study suggested there were markedly lower levels of
tubulin alpha 1b (TUBA1B) expression in BA 10, but not BA 9, from patients with
schizophrenia. We now use Western blotting to compare levels of TUBA1B
protein in BA 9 and 10 from patients with
schizophrenia and BA 10 from patients with
mood disorders to controls as well as in the frontal cortex from rats
after treatment with
haloperidol,
chlorpromazine or vehicle for 28 days. Levels of TUBA1B were significantly lower (- 18.6%) in BA 10, but not BA 9, from patients with
schizophrenia. Levels of TUBA1B did not differ significantly from controls in BA 10 from patients with
mood disorders or in the cortex of rats after
antipsychotic drug treatments. Levels of TUBA1B were significantly lower (- 30%) in BA 10 from patients with
schizophrenia who were not being treated with
antipsychotic drugs close to death compared to those who were treated close to death. These data suggest that lower levels of TUBA1B, a cytoskeletal
protein, in BA 10 from patients with
schizophrenia are not a simple
drug effect and therefore add to the hypothesis that a breakdown in cytoskeletal homoeostasis may be contributing to the genesis of the symptoms of the disorder.