Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
, 116, 57-67

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?

Affiliations
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.

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.

Similar articles

See all similar articles

Cited by 22 PubMed Central articles

See all "Cited by" articles

Substances

LinkOut - more resources

Feedback