A quantitative study on the expression of synapsin II and N-ethylmaleimide-sensitive fusion protein in schizophrenic

C Imai1, T Sugai, S Iritani

  • 1Molecular Neurobiology, Brain Research Institute, Niigata University, 951-8585, Niigata, Japan.

Neuroscience Letters
|June 19, 2001
PubMed

Insights

This study found no significant changes in synapsin II and N-ethylmaleimide-sensitive fusion protein (NSF) mRNA or protein levels in the prefrontal cortex of schizophrenia patients. These findings challenge previous reports and suggest a need for re-evaluation of molecular synaptic impairments in schizophrenia.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Schizophrenia is a complex psychiatric disorder with suspected neurochemical underpinnings.
  • Previous studies using DNA array technology suggested decreased expression of synapsin II and N-ethylmaleimide-sensitive fusion protein (NSF) mRNAs in schizophrenic patients' prefrontal cortex.

Purpose of the Study:

  • To investigate and reproduce the reported decrease in synapsin II and NSF expression in the prefrontal cortex of individuals with schizophrenia.
  • To validate findings using both mRNA and protein level measurements.

Main Methods:

  • Real-time polymerase chain reaction (PCR) was used to quantify mRNA levels of synapsin II and NSF.
  • Immunoblotting was employed to measure protein levels of synapsin II and NSF.
  • High-quality prefrontal cortex samples from schizophrenic patients and control subjects were analyzed.

Main Results:

  • Both real-time PCR and immunoblotting experiments showed no significant alteration in synapsin II and NSF mRNA or protein expression in the prefrontal cortex of schizophrenic samples compared to controls.
  • The findings contradict previous reports suggesting reduced expression of these presynaptic markers.

Conclusions:

  • The molecular impairments of synapses in schizophrenia may not be universally evident across all presynaptic markers.
  • Previous findings regarding synapsin II and NSF expression in schizophrenia require re-evaluation at the molecular level.

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