Evidence for glutamatergic neuronal dysfunction in the prefrontal cortex in chronic but not in first-episode patients with schizophrenia: a proton magnetic resonance spectroscopy study

Schizophr Res. 2005 Mar 1;73(2-3):153-7. doi: 10.1016/j.schres.2004.08.021.

Abstract

Based upon pharmacological challenge and postmortem studies, schizophrenia has been hypothesized to be caused by decreased glutamatergic neurotransmission. We investigated the glutamatergic neuronal metabolism of the dorsolateral prefrontal cortex with localized 1H magnetic resonance spectroscopy in 18 first-episode patients, 21 chronic patients with schizophrenia, and 21 age-matched controls. Chronic patients had significantly lower levels of glutamate/glutamine (Glx) and N-acetylaspartate (NAA) compared to healthy controls and first-episode patients. Reduced metabolite levels were not correlated with duration of illness or medication. Our results indicate glutamatergic dysfunction in chronic schizophrenia that could be evidence of a progressive brain disorder.

MeSH terms

  • Adult
  • Aspartic Acid / analogs & derivatives*
  • Aspartic Acid / metabolism*
  • Chronic Disease
  • Diagnostic and Statistical Manual of Mental Disorders
  • Female
  • Glutamic Acid / metabolism*
  • Glutamine / metabolism*
  • Humans
  • Magnetic Resonance Spectroscopy*
  • Male
  • Neurons / metabolism
  • Neurons / physiology*
  • Prefrontal Cortex / metabolism*
  • Prefrontal Cortex / physiopathology*
  • Protons*
  • Schizophrenia / diagnosis
  • Schizophrenia / metabolism*
  • Schizophrenia / physiopathology*
  • Schizophrenic Psychology
  • Severity of Illness Index
  • Synaptic Transmission / physiology*

Substances

  • Protons
  • Glutamine
  • Aspartic Acid
  • Glutamic Acid
  • N-acetylaspartate