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Brain Res. 2008 Jul 7;1218:267-77. doi: 10.1016/j.brainres.2008.03.092. Epub 2008 Apr 16.

Disease-specific alterations in glutamatergic neurotransmission on inhibitory interneurons in the prefrontal cortex in schizophrenia.

Author information

  • 1Laboratory for Structural and Molecular Neuroscience, McLean Hospital, Belmont, MA 02478, USA. wwoo@hms.harvard.edu

Abstract

Glutamatergic modulation of inhibitory interneurons plays a crucial role in shaping the flow of information in the cerebral cortex. In a cohort of postmortem human brains from schizophrenia (n=20), bipolar disorder (n=20) and normal control (n=20) subjects, we colocalized the mRNA for the N-methyl-d-aspartate (NMDA) receptor NR2A subunit, labeled with [35S], and the mRNA for the gamma-aminobutyric acid (GABA) synthesizing enzyme glutamic acid decarboxylase (GAD)67, labeled with digoxigenin. We found that the density of GAD67+ neurons in layers 2-5 of the prefrontal cortex was decreased by 27-36% in both schizophrenia and bipolar disorder. In addition, the density of the GAD67+/NR2A+ neurons was decreased by 57% and 49% in layers 3 and 4, respectively, in schizophrenia, but it was unchanged in bipolar disorder. These findings raise the possibility that glutamatergic innervation of inhibitory interneurons via the NMDA receptor in the prefrontal cortex may be selectively altered in schizophrenia.

PMID:
18534564
[PubMed - indexed for MEDLINE]
PMCID:
PMC2665281
Free PMC Article

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