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

Anthony J. Deo, Michael E. Cahill, Siyu Li, Isaac Goldszer, Ruth Henteleff, Jon Eric VanLeeuwen, Igor Rafalovich, Ruoqi Gao, Erin K. Stachowski, Allan R. Sampson, David A. Lewis, Peter Penzes, Robert A. Sweet*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

37 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)796-803
Number of pages8
JournalNeurobiology of Disease
Volume45
Issue number2
DOIs
StatePublished - Feb 2012

Keywords

  • Auditory cortex
  • Dendrite
  • Endophenotypes
  • Kalirin
  • Schizoaffective
  • Schizophrenia

ASJC Scopus subject areas

  • Neurology

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