Cited by 166Schizophrenia research and treatmentNeuroscience and Neuropharmacology ResearchAmino Acid Enzymes and Metabolism

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Assessment of Glutamate Transporter GLAST (EAAT1)-Deficient Mice for Phenotypes Relevant to the Negative and Executive/Cognitive Symptoms of Schizophrenia

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Karlsson, Rose-Marie, Tanaka, Kohichi, Saksida, Lisa M, Bussey, Timothy J, Heilig, Markus, Holmes, Andrew·2009·Neuropsychopharmacology

DOI 10.1038/npp.2008.215PMC PMC3400972

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Abstract

Glutamatergic dysfunction is increasingly implicated in the pathophysiology of schizophrenia. Current models postulate that dysfunction of glutamate and its receptors underlie many of the symptoms in this disease. However, the mechanisms involved are not well understood. Although elucidating the role for glutamate transporters in the disease has been limited by the absence of pharmacological tools that selectively target the transporter, we recently showed that glial glutamate and aspartate transporter (GLAST; excitatory amino-acid transporter 1) mutant mice exhibit abnormalities on behavioral measures thought to model the positive symptoms of schizophrenia, some of which were rescued by treatment with either haloperidol or the mGlu2/3 agonist, LY379268 the mGlu2/3 agonist, LY379268. To further determine the role of GLAST in schizophrenia-related behaviors we tested GLAST mutant mice on a series of behavioral paradigms associated with the negative (social withdrawal, anhedonia), sensorimotor gating (prepulse inhibition of startle), and executive/cognitive (discrimination learning, extinction) symptoms of schizophrenia. GLAST knockout (KO) mice showed poor nesting behavior and abnormal sociability, whereas KO and heterozygous (HET) both demonstrated lesser preference for a novel social stimulus compared to wild-type littermate controls. GLAST KO, but not HET, had a significantly reduced acoustic startle response, but no significant deficit in prepulse inhibition of startle. GLAST KO and HET showed normal sucrose preference. In an instrumental visual discrimination task, KO showed impaired learning. By contrast, acquisition and extinction of a simple instrumental response was normal. The mGlu2/3 agonist, LY379268, failed to rescue the discrimination impairment in KO mice. These findings demonstrate that gene deletion of GLAST produces select phenotypic abnormalities related to the negative and cognitive symptoms of schizophrenia.

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Authors: Karlsson, R.-M., Tanaka, K., Saksida, L. M., Bussey, T. J., Heilig, M., & Holmes, A.
Affiliations: National Institutes of Health (US)
Tokyo Medical and Dental University (JP)
University of Cambridge (GB)
Corresponding author: Karlsson, Rose-Marie
ORCID: Tanaka, Kohichi
Saksida, Lisa M
Bussey, Timothy J
Heilig, Markus
Holmes, Andrew
Venue: Neuropsychopharmacology
Publisher: Springer Science and Business Media LLC
Published: 2008-12-10
Volume: 34
Issue: 6
Pages: 1578-1589
ISSN: 0893-133X (ISSN-L)
1740-634X
DOI: 10.1038/npp.2008.215
PMC: PMC3400972
OpenAlex: W2084421163
Cited by: 165
References: 66
Citations by year: 2026: 3 · 2025: 5 · 2024: 7 · 2023: 4 · 2022: 7 · 2021: 9 · 2020: 6 · 2019: 9 · 2018: 11 · 2017: 5 · 2016: 10 · 2015: 12 · 2014: 11 · 2013: 17 · 2012: 16
FWCI: 7.73
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Neuropsychopharmacology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Johns Hopkins University
Novartis Foundation
Tokyo Biochemical Research Foundation
NOVARTIS Foundation (Japan) for the Promotion of Science
Research Foundation for Opto-Science and Technology
National Institutes of Health
Japan Society for the Promotion of Science (20022013, 18053006)
National Institute on Alcohol Abuse and Alcoholism (ZIAAA000411)
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 › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
Keywords: GLAST, glutamate transporters, schizophrenia, negative symptoms, cognitive symptoms, prepulse inhibition, acoustic startle response, social withdrawal, anhedonia, visual discrimination learning, extinction learning, LY379268, haloperidol, knockout mice
MeSH terms: Amino Acids, Animals, Cognition, Cognition Disorders, Disease Models, Animal, Female, Food Preferences, Learning, Male, Mice, Inbred C57BL, Mice, Transgenic, Motor Activity, Phenotype, Schizophrenia, Social Behavior Disorders, Reflex, Startle, Sucrose, Receptors, Metabotropic Glutamate, Bridged Bicyclo Compounds, Heterocyclic, Excitatory Amino Acid Transporter 1, Mice

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Assessment of Glutamate Transporter GLAST (EAAT1)-Deficient Mice for Phenotypes Relevant to the Negative and Executive/Cognitive Symptoms of Schizophrenia

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