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Dysbindin-1 modulates prefrontal cortical activity and schizophrenia-like behaviors via dopamine/D2 pathways

F Papaleo1, F Yang, S Garcia

  • 1Clinical Brain Disorders Branch, Genes, Cognition and Psychosis Program, National Institute of Mental Health, Bethesda, MD 20892, USA. francesco.papaleo@iit.it

Molecular Psychiatry
|October 20, 2010
PubMed

Insights

Dysbindin-1 deficiency in mice alters dopamine-related behaviors and impairs working memory, particularly under stress. This study reveals molecular and cellular changes in the medial prefrontal cortex linked to psychosis.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Dysbindin-1 is linked to schizophrenia and regulates dopamine D2-receptor trafficking.
  • The precise molecular mechanisms connecting dysbindin-1 to schizophrenia's clinical symptoms remain unclear.

Purpose of the Study:

  • To investigate the role of dysbindin-1 in schizophrenia-related behaviors, medial prefrontal cortex (mPFC) function, and D2-receptor signaling in mice.
  • To explore how dysbindin-1 deficiency affects neural excitability and molecular pathways in the mPFC.

Main Methods:

  • Utilized dysbindin-1-deficient mice (dys-/-) to assess behavioral phenotypes.
  • Examined molecular and electrophysiological changes in the mPFC.
  • Investigated the impact of D2-receptor stimulation on behavior and neural activity.

Main Results:

  • Dysbindin-1 disruption altered dopamine-related behaviors and impaired working memory under stress.
  • Pyramidal neurons in the mPFC of dys-/- mice showed altered excitability.
  • Reduced expression of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and CaMKKβ was observed in the mPFC of dys-/- mice.
  • D2-receptor agonist treatment mimicked some molecular and behavioral effects.

Conclusions:

  • Dysbindin-1 modulates D2-receptor-related behaviors and cortical activity.
  • Cellular and molecular changes in the mPFC, including CaMK pathways, are implicated in the association between dysbindin-1 and psychosis.
  • Findings provide insights into the neurobiological underpinnings of schizophrenia.

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