Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
16
pubmed:dateCreated
2001-8-6
pubmed:abstractText
Systemic administration of the glutamic acid analog kainic acid (KA) causes neuronal cell death in brain-vulnerable regions, such as the piriform cortex, hippocampus, and amygdala in rats. We investigated the relationship between the KA-induced neuronal apoptosis and expression of cyclin-dependent kinase 4 (CDK4) and cyclin D1, key regulators of cell cycle progression. Expression of CDK4 and cyclin D1 was upregulated in neurons of the rat piriform cortex and amygdala 1-3 d after KA administration in vivo. CDK4 and cyclin D1 proteins were induced in the cytoplasm and nuclei of neurons, with a concomitant increase of CDK4- and cyclin D1-positive microglia in the affected areas. Continuous infusion of 100 microm CDK4 or cyclin D1 antisense oligonucleotides into the lateral ventricle using mini-osmotic pumps suppressed the excitotoxin-induced neuronal cell death in the piriform cortex and basolateral amygdaloid nucleus, whereas sense oligonucleotides exhibited no such effect. Although KA administration causes prolonged c-Fos expression in the vulnerable regions that preceded the induction of neuronal apoptosis, the CDK4 or cyclin D1 antisense oligonucleotides exhibited no suppressive effect on c-Fos levels. Our results suggest that CDK4 and cyclin D1 are essential for KA-induced neuronal apoptosis in vivo.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6086-94
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11487632-Amygdala, pubmed-meshheading:11487632-Animals, pubmed-meshheading:11487632-Antigens, Differentiation, pubmed-meshheading:11487632-Apoptosis, pubmed-meshheading:11487632-Cerebral Cortex, pubmed-meshheading:11487632-Cyclin D1, pubmed-meshheading:11487632-Cyclin-Dependent Kinase 4, pubmed-meshheading:11487632-Cyclin-Dependent Kinases, pubmed-meshheading:11487632-Hippocampus, pubmed-meshheading:11487632-In Situ Hybridization, pubmed-meshheading:11487632-In Situ Nick-End Labeling, pubmed-meshheading:11487632-Injections, Intraventricular, pubmed-meshheading:11487632-Kainic Acid, pubmed-meshheading:11487632-Male, pubmed-meshheading:11487632-Microglia, pubmed-meshheading:11487632-Neurons, pubmed-meshheading:11487632-Olfactory Pathways, pubmed-meshheading:11487632-Oligonucleotides, Antisense, pubmed-meshheading:11487632-Proto-Oncogene Proteins, pubmed-meshheading:11487632-Proto-Oncogene Proteins c-fos, pubmed-meshheading:11487632-RNA, Messenger, pubmed-meshheading:11487632-Rats, pubmed-meshheading:11487632-Rats, Sprague-Dawley, pubmed-meshheading:11487632-Up-Regulation
pubmed:year
2001
pubmed:articleTitle
Cyclin-dependent kinase 4 and cyclin D1 are required for excitotoxin-induced neuronal cell death in vivo.
pubmed:affiliation
Department of Neurobiology (C1), Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. ino@med.m.chiba-u.ac.jp
pubmed:publicationType
Journal Article