A quantitative review of the postmortem evidence for decreased cortical N-methyl-D-aspartate receptor expression levels in schizophrenia: How can we link molecular abnormalities to mismatch negativity deficits?

Vibeke S Catts¹, Yan Ling Lai², Cyndi Shannon Weickert³, Thomas W Weickert³, Stanley V Catts⁴

Affiliations

¹ Schizophrenia Research Institute, Sydney, Australia; Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; School of Psychiatry, University of New South Wales, Sydney, Australia. Electronic address: v.catts@NeuRA.edu.AU.
² Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; Faculty of Medicine, University of New South Wales, Sydney, Australia.
³ Schizophrenia Research Institute, Sydney, Australia; Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; School of Psychiatry, University of New South Wales, Sydney, Australia.
⁴ Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; Discipline of Psychiatry, University of Queensland, Brisbane, Australia; Brain and Mind Research Institute, University of Sydney, Sydney, Australia.

PMID: 26549579
DOI: 10.1016/j.biopsycho.2015.10.013

Free article

Review

A quantitative review of the postmortem evidence for decreased cortical N-methyl-D-aspartate receptor expression levels in schizophrenia: How can we link molecular abnormalities to mismatch negativity deficits?

Vibeke S Catts et al. Biol Psychol. 2016 Apr.

Free article

. 2016 Apr:116:57-67.

doi: 10.1016/j.biopsycho.2015.10.013. Epub 2015 Nov 10.

Authors

Vibeke S Catts¹, Yan Ling Lai², Cyndi Shannon Weickert³, Thomas W Weickert³, Stanley V Catts⁴

Affiliations

¹ Schizophrenia Research Institute, Sydney, Australia; Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; School of Psychiatry, University of New South Wales, Sydney, Australia. Electronic address: v.catts@NeuRA.edu.AU.
² Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; Faculty of Medicine, University of New South Wales, Sydney, Australia.
³ Schizophrenia Research Institute, Sydney, Australia; Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; School of Psychiatry, University of New South Wales, Sydney, Australia.
⁴ Schizophrenia Research Laboratory, Neuroscience Research Australia, Sydney, Australia; Discipline of Psychiatry, University of Queensland, Brisbane, Australia; Brain and Mind Research Institute, University of Sydney, Sydney, Australia.

PMID: 26549579
DOI: 10.1016/j.biopsycho.2015.10.013

Abstract

Evidence suggests that anomalous mismatch negativity (MMN) in schizophrenia is related to glutamatergic abnormalities, possibly involving N-methyl-D-aspartate (NMDA) receptors. Decreased cortical expressions of NMDA receptor subunits have been observed in schizophrenia, though not consistently. To aid with integration and interpretation of previous work, we performed a meta-analysis of effect sizes of mRNA or protein levels of the obligatory NR1 subunit in prefrontal cortex from people with schizophrenia. In schizophrenia compared to unaffected controls the pooled effect size was -0.64 (95% confidence interval: -1.08 to -0.20) for NR1 mRNA reduction and -0.44 (95% confidence interval: -0.80 to -0.07) for NR1 protein reduction. These results represent the first step to a deeper understanding of the region-specific, cell-specific, and stage-specific NMDA receptor hypofunction in schizophrenia, which could be linked to mismatch negativity deficits via transgenic and pharmacological animal models.

Keywords: Glutamate; Meta-analysis; Mismatch negativity; NMDA receptor; Prefrontal cortex; Schizophrenia.

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A quantitative review of the postmortem evidence for decreased cortical N-methyl-D-aspartate receptor expression levels in schizophrenia: How can we link molecular abnormalities to mismatch negativity deficits?

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A quantitative review of the postmortem evidence for decreased cortical N-methyl-D-aspartate receptor expression levels in schizophrenia: How can we link molecular abnormalities to mismatch negativity deficits?

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