Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-3-18
pubmed:abstractText
Glutamate excitotoxicity plays a key role in inducing neuronal cell death in many neurological diseases. In mice, administration of kainic acid, an analogue of the excitotoxin glutamate, results in hippocampal cell death and seizures. Kainic-acid-induced seizures in mice provide a well-characterized model for studies of human neurodegenerative diseases. However, C57BL/6 mice, which are often used for genetic analyses and transgenic and knockout studies, are resistant to excitotoxicity induced by subcutaneous administration of kainic acid. In the present study, kainic acid administered by the intranasal route was shown to result in continuous tonic-clonic seizures in C57BL/6 mice. These seizures continued for 1-5 h and successfully induced selective lesions in area CA3 of the hippocampus. The survival rate was high even after mice experienced severe seizures. The hippocampal lesions were associated with a high level of cyclooxygenase-2 production as well as astrogliosis. Administration of kainic acid also altered behavioral responses, with mice showing a significant increase in locomotion and rearing activity as indicated by an open-field test. This animal model could provide a valuable tool for exploring the role of excitotoxicity in neuropathological conditions and should be further evaluated in gene-targeting studies of neurodegenerative diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
931
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
135-45
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11897099-Administration, Intranasal, pubmed-meshheading:11897099-Age Factors, pubmed-meshheading:11897099-Animals, pubmed-meshheading:11897099-Apoptosis, pubmed-meshheading:11897099-Behavior, Animal, pubmed-meshheading:11897099-Body Weight, pubmed-meshheading:11897099-Cyclooxygenase 2, pubmed-meshheading:11897099-Disease Models, Animal, pubmed-meshheading:11897099-Dose-Response Relationship, Drug, pubmed-meshheading:11897099-Excitatory Amino Acid Agonists, pubmed-meshheading:11897099-Gliosis, pubmed-meshheading:11897099-Hippocampus, pubmed-meshheading:11897099-Immunohistochemistry, pubmed-meshheading:11897099-Isoenzymes, pubmed-meshheading:11897099-Kainic Acid, pubmed-meshheading:11897099-Mice, pubmed-meshheading:11897099-Mice, Inbred C57BL, pubmed-meshheading:11897099-Neurodegenerative Diseases, pubmed-meshheading:11897099-Neurons, pubmed-meshheading:11897099-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:11897099-Seizures, pubmed-meshheading:11897099-Survival Rate
pubmed:year
2002
pubmed:articleTitle
Excitotoxic neurodegeneration induced by intranasal administration of kainic acid in C57BL/6 mice.
pubmed:affiliation
NEUROTEC, Division of Experimental Geriatrics, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't