Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-7-2
pubmed:abstractText
Glutamate released by activated microglia induces excito-neurotoxicity and may contribute to neurodegeneration in numerous neurological diseases including ischemia, inflammation, epilepsy, and neurodegenerative diseases. We observed that the gap junction blocker carbenoxolone (CBX) or the glutaminase inhibitor 6-diazo-5-oxo-L-norleucine (DON) decreased glutamate release from activated microglia and rescued neuronal death in a dose-dependent manner in vitro. In gerbils, treatment with CBX or DON also prevented the delayed death of hippocampal neurons following transient global ischemia. Thus, blockade of microglial glutamate release may be an effective therapeutic strategy against neurodegeneration after ischemic injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1090-2430
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
214
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
144-6
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Blockade of microglial glutamate release protects against ischemic brain injury.
pubmed:affiliation
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan. htake@riem.nagoya-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't