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Altered Rbfox1-Vamp1 pathway and prefrontal cortical dysfunction in schizophrenia.

Youjin Chung1, Samuel J Dienel1,2, Matthew J Belch1

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Schizophrenia is linked to lower Rbfox1 protein and Vamp1 mRNA in brain cells, impairing cortical inhibition and gamma oscillations. This suggests the Rbfox1-Vamp1 pathway contributes to schizophrenia

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Deficient gamma oscillations in the prefrontal cortex (PFC) are observed in schizophrenia, linked to impaired inhibitory drive from parvalbumin-expressing interneurons (PVIs).
  • RNA binding fox-1 homolog 1 (Rbfox1) regulates PVI inhibitory drive, with its cytoplasmic isoform affecting target mRNA stability, including vesicle associated membrane protein 1 (Vamp1).
  • Vamp1 mediates GABA release probability from PVIs, and Rbfox1 loss reduces Vamp1, impairing cortical inhibition.

Purpose of the Study:

  • To investigate alterations in the Rbfox1-Vamp1 pathway within PVIs in the PFC of individuals with schizophrenia.
  • To determine the functional impact of these alterations on gamma oscillations using computational modeling.

Main Methods:

  • Multi-label in situ hybridization and immunohistochemistry were used on PFC tissue from 20 matched pairs of schizophrenia and comparison subjects.
  • Cytoplasmic Rbfox1 protein and Vamp1 mRNA levels were quantified in PVIs.
  • A computational network model simulated the effect of reduced GABA release probability on gamma power.

Main Results:

  • Significantly lower cytoplasmic Rbfox1 protein levels were found in PVIs from individuals with schizophrenia.
  • Vamp1 mRNA levels were also significantly lower in schizophrenia PVIs and correlated with Rbfox1 protein levels.
  • Computational simulations demonstrated that reduced GABA release probability decreases gamma power by disrupting network synchrony.

Conclusions:

  • The Rbfox1-Vamp1 pathway in PVIs is impaired in schizophrenia.
  • This impairment likely contributes to the deficient PFC gamma oscillations observed in the illness.
  • Findings highlight a novel molecular mechanism underlying cognitive deficits in schizophrenia.