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Relationship between somatostatin and death receptor expression in the orbital frontal cortex in schizophrenia: a

Dipesh Joshi1, Vibeke S Catts1, Juan C Olaya1

  • 1Schizophrenia Research Institute, Liverpool Street, Darlinghurst, NSW, Australia; Neuroscience Research Australia, Barker Street, Randwick, NSW, Australia; School of Psychiatry, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.

NPJ Schizophrenia
|June 24, 2016
PubMed
Abstract

Insights

Schizophrenia involves reduced somatostatin (SST) mRNA in the orbital frontal cortex (OFC), particularly in layer II. This deficit correlates with increased cell death signaling, suggesting SST interneurons are vulnerable in this condition.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Molecular Biology

Background:

  • Previous research indicated reduced GAD67 and Dlx mRNAs in the orbital frontal cortex (OFC) of individuals with schizophrenia.
  • It was unclear if these reductions were primarily due to changes in somatostatin (SST) or parvalbumin (PV) mRNA expression, or decreased SST mRNA-positive interneuron density.

Purpose of the Study:

  • To ascertain if inhibitory interneuron deficits in the OFC of individuals with schizophrenia are more pronounced for SST or PV mRNAs.
  • To investigate whether these deficits correlate with mRNAs encoding cell death signaling molecules.

Main Methods:

  • Inhibitory interneuron mRNAs (SST, PV) and death signaling mRNAs (FAS receptor (FASR), TNFSF13) were quantified using in situ hybridization and quantitative PCR (qPCR) in control and schizophrenia subjects.
  • SST mRNA-positive interneuron-like cells were counted in layer II of the gyrus rectus.
  • Gray matter SST and PV mRNAs were correlated with interstitial white matter neuron (IWMN) density and death signaling mRNAs.

Main Results:

  • SST mRNA was significantly reduced in all OFC layers in schizophrenia, with the greatest reduction (67%) in layer II.
  • Layer II SST mRNA-positive neuron density decreased by approximately 29% in schizophrenia.
  • PV mRNA showed reductions in layers III and IV, but no significant diagnostic difference was found via qPCR.
  • FASR mRNA levels were elevated by 34% in schizophrenia.
  • SST expression, unlike PV, correlated negatively with FASR and TNFSF13 expressions and with IWMN density.

Conclusions:

  • The study identifies SST interneurons as predominantly linked to inhibitory interneuron pathology in the OFC in schizophrenia.
  • Increased death receptor signaling mRNAs are associated with prominent laminar deficits in SST mRNA within the OFC in schizophrenia.
  • SST interneurons appear more susceptible to increased death receptor signaling compared to PV interneurons in schizophrenia.

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