Modeling interneuron dysfunction in schizophrenia.

Developmental Neuroscience
Martin J Schmidt, Karoly Mirnics

Abstract

Schizophrenia is a debilitating neurodevelopmental disorder affecting approximately 1% of the population and imposing a significant burden on society. One of the most replicated and well-established postmortem findings is a deficit in the expression of the gene encoding the 67-kDa isoform of glutamic acid decarboxylase (GAD67), the primary GABA-producing enzyme in the brain. GAD67 is expressed in various classes of interneurons, with vastly different morphological, molecular, and physiological properties. Importantly, GABA system deficits in schizophrenia encompass multiple interneuronal subtypes, raising several important questions. First, do different classes of interneurons regulate different aspects of behavior? Second, can we model cell-type-specific GABAergic deficits in mice, and will the rodent findings translate to human physiology? Finally, will this knowledge open the door to knowledge-based approaches to treat schizophrenia?

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Citations

Sep 13, 2012·European Archives of Psychiatry and Clinical Neuroscience·Nina PeselmannMathias Zink
Jul 19, 2013·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Rahul BharadwajSchahram Akbarian
Feb 9, 2016·Neuroscience·S KálmánK Mirnics
Jan 28, 2015·Molecular Psychiatry·J A BrownKároly Mirnics
Apr 8, 2015·Neurobiology of Learning and Memory·Hirofumi MorishitaSchahram Akbarian
Nov 19, 2013·Neurobiology of Disease·Jacquelyn A BrownKároly Mirnics
Apr 25, 2014·Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology·Martin J Schmidt, Karoly Mirnics
Feb 19, 2021·Brain Research·Allison AndersonKaroly Mirnics

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