GAD67: the link between the GABA-deficit hypothesis and the dopaminergic- and glutamatergic theories of psychosis

@article{Kalkman2003GAD67TL,
  title={GAD67: the link between the GABA-deficit hypothesis and the dopaminergic- and glutamatergic theories of psychosis},
  author={Hans Otto Kalkman and Erika Loetscher},
  journal={Journal of Neural Transmission},
  year={2003},
  volume={110},
  pages={803-812}
}
Summary. Decreases in the 67 kDa isoenzyme of brain glutamic acid decarboxylase (GAD67) expression have been consistently found in patients with bipolar disorder and schizophrenia. In animals GAD67 expression is diminished by chronic, but not acute stimulation of dopamine D2 receptors and by short-term blockade of NMDA receptors. In contrast, chronic treatment with D2 receptor antagonists enhances GAD67 expression. Thus, antipsychotic treatment cannot explain the reduction in GAD67 levels in… 
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