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Postsynaptic Density-95 Isoform Abnormalities in Schizophrenia.

Adam J Funk1, Catharine A Mielnik2, Rachael Koene1

  • 1Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH.

Schizophrenia Bulletin
|January 28, 2017
PubMed
Summary
This summary is machine-generated.

Schizophrenia is linked to altered expression of specific Postsynaptic density-95 (PSD-95) splice variants, impacting synaptic function. These changes were observed in human brain tissue and validated in mouse models, suggesting a complex role for PSD-95 in the disease.

Keywords:
PSD-95isoformmRNApostmortemproteinschizophreniasplice variant

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Postsynaptic density-95 (PSD-95) protein expression is altered in schizophrenia across various brain regions.
  • Specific PSD-95 mRNA splice variants may play a critical role in the pathophysiology of schizophrenia.

Purpose of the Study:

  • To investigate PSD-95 mRNA splice variant expression in the dorsolateral prefrontal cortex of individuals with schizophrenia.
  • To correlate PSD-95 expression patterns with schizophrenia, antipsychotic treatment, and N-methyl-d-aspartate receptor (NMDAR) function.

Main Methods:

  • Quantitative PCR and Western blot analysis were employed to measure PSD-95 expression.
  • Studies included postmortem brain tissue from schizophrenia patients and controls, rodent models (haloperidol treatment, GluN1 knockdown), and postmortem interval assessments.

Main Results:

  • Decreased mRNA expression of PSD-95 beta and truncated isoforms was observed in schizophrenia patients.
  • PSD-95 protein levels were also reduced in schizophrenia subjects.
  • PSD-95 beta transcript increased in GluN1 knockdown mice, while alpha mRNA increased in rats after haloperidol treatment.

Conclusions:

  • Specific PSD-95 isoform dysregulation is implicated in schizophrenia, chronic neuroleptic treatment, and NMDAR deficiency models.
  • These findings suggest isoform-specific regulation of PSD-95 is crucial for synaptic signaling, potentially affecting NMDAR and AMPA receptor function.
  • Disruptions in excitatory signaling complexes via genetic, pharmacologic, or disease mechanisms specifically alter PSD-95 expression.