Cited by 184Schizophrenia research and treatmentNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

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Glutamatergic Synaptic Dysregulation in Schizophrenia: Therapeutic Implications

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Coyle, Joseph T., Basu, Alo, Benneyworth, Michael, Balu, Darrick, Konopaske, Glenn·2012·Handbook of Experimental Pharmacology

DOI 10.1007/978-3-642-25758-2_10PMC PMC4817347

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Abstract

Schizophrenia affects approximately 1% of the population and continues to be associated with poor outcome because of the limited efficacy of and noncompliance with existing antipsychotic medications. An alternative hypothesis invoking the excitatory neurotransmitter, glutamate, arose out of clinical observations that NMDA receptor antagonists, the dissociative anesthetics like ketamine, can replicate in normal individuals the full range of symptoms of schizophrenia including psychosis, negative symptoms, and cognitive impairments. Low dose ketamine can also re-create a number of physiologic abnormalities characteristic of schizophrenia. Postmortem studies have revealed abnormalities in endogenous modulators of NMDA receptors in schizophrenia as well as components of a postsynaptic density where NMDA receptors are localized. Gene association studies have revealed several genes that affect NMDA receptor function whose allelic variants are associated with increased risk for schizophrenia including genes encoding D-amino acid oxidase, its modulator G72, dysbindin, and neuregulin. The parvalbumin-positive, fast-firing GABAergic interneurons that provide recurrent inhibition to cortical-limbic pyramidal neurons seem to be most sensitive to NMDA receptor hypofunction. As a consequence, disinhibition of glutamatergic efferents disrupts cortical processing, causing cognitive impairments and negative symptoms, and drives subcortical dopamine release, resulting in psychosis. Drugs designed to correct the cortical-limbic dysregulated glutamatergic neurotransmission show promise for reducing negative and cognitive symptoms of schizophrenia as well as its positive symptoms.

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Authors: Coyle, J. T., Basu, A., Benneyworth, M., Balu, D., & Konopaske, G.
Affiliations: Harvard University (US)
Corresponding author: Coyle, Joseph T.
ORCID: Coyle, Joseph T.
Benneyworth, Michael
Balu, Darrick
Venue: Handbook of Experimental Pharmacology
Publisher: Springer Berlin Heidelberg
Published: 2012
Issue: 213
Pages: 267-295
ISSN: 0171-2004 (ISSN-L)
1865-0325
DOI: 10.1007/978-3-642-25758-2_10
PMC: PMC4817347
OpenAlex: W1872072116
Cited by: 180
References: 216
Citations by year: 2026: 7 · 2025: 7 · 2024: 6 · 2023: 4 · 2022: 13 · 2021: 19 · 2020: 10 · 2019: 9 · 2018: 10 · 2017: 11 · 2016: 11 · 2015: 21 · 2014: 25 · 2013: 22 · 2012: 4
FWCI: 81.63
Type: book chapter
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Handbook of experimental pharmacology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: U.S. Public Health Service
National Institute of Mental Health (P50MH060450, R01 MH51290, R01MH051290, F32MH090697, P50MH06045)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords: schizophrenia, NMDA receptor hypofunction, ketamine, dissociative anesthetics, postsynaptic density, D-amino acid oxidase, G72, dysbindin, neuregulin, parvalbumin interneurons, cognitive impairment, negative symptoms, psychosis, dopamine release, glutamatergic neurotransmission
MeSH terms: Animals, Cognition, gamma-Aminobutyric Acid, Humans, Ketamine, Synaptic Transmission, Schizophrenia, Synapses, Receptors, N-Methyl-D-Aspartate, Glutamic Acid

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Glutamatergic Synaptic Dysregulation in Schizophrenia: Therapeutic Implications

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