Increased expression of Kalirin-9 in the auditory cortex of schizophrenia subjects: Its role in dendritic pathology

Neurobiology of Disease

Robert A. Sweet¹  Michael E. Cahill²  Allan R. Sampson³  Ruoqi Gao⁴  Igor Rafalovich⁴  Siyu Li⁴  Erin K. Stachowski⁴  David A. Lewis⁵  Isaac Goldszer⁵  Anthony J. Deo⁶  Ruth Henteleff⁶  Jon-Eric VanLeeuwen⁶  Peter Penzes⁶ 

[1] Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA;Physician Scientist Training Program, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA;Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA;Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA;Department of Statistics, University of Pittsburgh, Pittsburgh, PA, USA;Translational Neuroscience Program, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA;

关键词: Endophenotypes;    Kalirin;    Schizophrenia;    Schizoaffective;    Auditory cortex;    Dendrite;   

DOI  :  

来源: DOAJ

【 摘 要 】

Reductions in dendritic arbor length and complexity are among the most consistently replicated changes in neuronal structure in post mortem studies of cerebral cortical samples from subjects with schizophrenia, however, the underlying molecular mechanisms have not been identified. This study is the first to identify an alteration in a regulatory protein which is known to promote both dendritic length and arborization in developing neurons, Kalirin-9. We found Kalirin-9 expression to be paradoxically increased in schizophrenia. We followed up this observation by overexpressing Kalirin-9 in mature primary neuronal cultures, causing reduced dendritic length and complexity. Kalirin-9 overexpression represents a potential mechanism for dendritic changes seen in schizophrenia.

【 授权许可】

Unknown