Reduced microglial immunoreactivity for endogenous NMDA receptor agonist quinolinic acid in the hippocampus of schizophrenia patients

We postulated that the previously mentioned glutamatergic impairments in the hippocampus of schizophrenia patients may be related to the microglial synthesis of quinolinic acid (QUIN), an endogenous N-methyl-d-aspartate receptor (NMDAR) agonist. Reduced microglial immunoreactivity for endogenous NMDA receptor agonist quinolinic acid in the hippocampus of schizophrenia patients. We measured the number of QUIN-immunoreactivity microglial cells in the CA1, CA2/3, and dentate gyrus (DG) regions of the posterior hippocampus formation in schizophrenia patients and matched controls. HLA-DR, a popular microglial surface marker, was further immunostained in nearby histological sections. In the CA1 hippocampus sub region of schizophrenia patients compared to controls, fewer QUIN-immunoreactivity microglial cells were seen (left p=0.028, right p=0.018). In the CA2/3 and DG areas, no notable diagnosis-dependent alterations were seen. Potential confounding factors such as age, disease duration, autolysis time, psychotropic medication, and hippocampus volume were taken into account while analyzing these results. There were no variations in the overall density of microglial cells linked to diagnosis (HLA-DR expression). Our results imply that schizophrenia is related with decreased microglial QIUN content in the hippocampus CA1 region. We surmise that this connection could be a factor in schizophrenia patients' hippocampus' decreased glutamatergic neurotransmission.

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