Glutamatergic Animal Models of Schizophrenia

Bita Moghaddam, Mark E. Jackson

Research output: Contribution to journalArticle

113 Citations (Scopus)

Abstract

Several lines of evidence, including recent genetic linkage studies implicating susceptibility genes for schizophrenia, make a strong case that abnormal NMDA receptor-mediated neurotransmission is a major locus for the pathophysiology of schizophrenia. Animal models that are relevant to putative NMDA dysfunction in schizophrenia have excellent face validity for several symptoms of schizophrenia and are important tools for the design of novel pharmacological intervention in schizophrenia. The present chapter includes a brief review of the utility of these models and the search for new medications that have the potential of normalizing glutamate neurotransmission in schizophrenia.

Original languageEnglish (US)
Pages (from-to)131-137
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume1003
DOIs
StatePublished - Nov 2003
Externally publishedYes

Fingerprint

Schizophrenia
Animals
Animal Models
N-Methylaspartate
N-Methyl-D-Aspartate Receptors
Glutamic Acid
Genes
Synaptic Transmission
Genetic Linkage
Reproducibility of Results
Animal Model
Pharmacology

Keywords

  • Cognitions
  • Dopamine
  • NMDA receptors
  • Prefrontal cortex
  • Schizophrenia

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Glutamatergic Animal Models of Schizophrenia. / Moghaddam, Bita; Jackson, Mark E.

In: Annals of the New York Academy of Sciences, Vol. 1003, 11.2003, p. 131-137.

Research output: Contribution to journalArticle

@article{afbe72cac8bc46e792abdad33caebe5b,
title = "Glutamatergic Animal Models of Schizophrenia",
abstract = "Several lines of evidence, including recent genetic linkage studies implicating susceptibility genes for schizophrenia, make a strong case that abnormal NMDA receptor-mediated neurotransmission is a major locus for the pathophysiology of schizophrenia. Animal models that are relevant to putative NMDA dysfunction in schizophrenia have excellent face validity for several symptoms of schizophrenia and are important tools for the design of novel pharmacological intervention in schizophrenia. The present chapter includes a brief review of the utility of these models and the search for new medications that have the potential of normalizing glutamate neurotransmission in schizophrenia.",
keywords = "Cognitions, Dopamine, NMDA receptors, Prefrontal cortex, Schizophrenia",
author = "Bita Moghaddam and Jackson, {Mark E.}",
year = "2003",
month = "11",
doi = "10.1196/annals.1300.065",
language = "English (US)",
volume = "1003",
pages = "131--137",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Glutamatergic Animal Models of Schizophrenia

AU - Moghaddam, Bita

AU - Jackson, Mark E.

PY - 2003/11

Y1 - 2003/11

N2 - Several lines of evidence, including recent genetic linkage studies implicating susceptibility genes for schizophrenia, make a strong case that abnormal NMDA receptor-mediated neurotransmission is a major locus for the pathophysiology of schizophrenia. Animal models that are relevant to putative NMDA dysfunction in schizophrenia have excellent face validity for several symptoms of schizophrenia and are important tools for the design of novel pharmacological intervention in schizophrenia. The present chapter includes a brief review of the utility of these models and the search for new medications that have the potential of normalizing glutamate neurotransmission in schizophrenia.

AB - Several lines of evidence, including recent genetic linkage studies implicating susceptibility genes for schizophrenia, make a strong case that abnormal NMDA receptor-mediated neurotransmission is a major locus for the pathophysiology of schizophrenia. Animal models that are relevant to putative NMDA dysfunction in schizophrenia have excellent face validity for several symptoms of schizophrenia and are important tools for the design of novel pharmacological intervention in schizophrenia. The present chapter includes a brief review of the utility of these models and the search for new medications that have the potential of normalizing glutamate neurotransmission in schizophrenia.

KW - Cognitions

KW - Dopamine

KW - NMDA receptors

KW - Prefrontal cortex

KW - Schizophrenia

UR - http://www.scopus.com/inward/record.url?scp=0347091934&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0347091934&partnerID=8YFLogxK

U2 - 10.1196/annals.1300.065

DO - 10.1196/annals.1300.065

M3 - Article

C2 - 14684441

AN - SCOPUS:0347091934

VL - 1003

SP - 131

EP - 137

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -