Linked Life Data

11506886

Source:http://linkedlifedata.com/resource/pubmed/id/11506886

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2001-8-16
pubmed:abstractText
The neurobiology of schizophrenia remains poorly understood. Symptoms of schizophrenia are classically thought to be associated with an imbalance of the dopaminergic system. However, the contribution of other neurotransmitters, in particular glutamate, has been increasingly appreciated. The role of individual components of neurotransmitter systems in aberrant behaviors can be experimentally tested in transgenic animals. Dopamine transporter knockout mice display persistently elevated dopaminergic tone and therefore might be appropriate substrates to evaluate the dopamine hypothesis. Similarly, NMDA receptor-deficient mice can be used to evaluate the glutamate hypothesis of schizophrenia. In this review we discuss how such animal models might be relevant for understanding the neurochemical underpinnings of certain manifestations of schizophrenia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0166-2236
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
527-33
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Genetic animal models: focus on schizophrenia.
pubmed:affiliation
Howard Hughes Medical Institute Laboratories, Dept. of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Review