Abstract
Translational studies are becoming more common in schizophrenia research. The past couple of decades witnessed the emergence of novel ideas regarding schizophrenia pathophysiology that originated from both human and animal studies. The findings that glutamate and gamma-aminobutyric acid transmission are affected in the disease led to the hypothesis of altered inhibitory neurotransmission as critical for cognitive deficits and to an exploration of novel therapeutic approaches aimed at restoring excitation-inhibition balance. Much is to be done yet to elucidate the ultimate mechanisms by which excitation and inhibition are affected in this disorder; a comprehensive translational effort is necessary to address what may cause altered GABA function, for example. Here, we present an overview of the excitation-inhibition imbalance hypothesis in schizophrenia and discuss ongoing efforts aimed at determining whether cortical inhibitory interneurons are affected by oxidative stress during development.