Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-7-20
pubmed:abstractText
Glycogen synthase kinase 3beta (GSK3beta) is believed to play important roles in the regulation of synaptic plasticity, cell survival and circadian rhythms in the mature CNS. However, although several studies have been focused on the GSK3beta, little is known about GSK3beta changes in glial cells under neuropathological conditions. In this study, we evaluated the expressions of molecules associated with the GSK3beta signaling pathway, following the induction of an excitotoxic lesion in mouse brain by kainic acid (KA) injection, which caused pyramidal cell degeneration in the hippocampal CA3 region. In injured hippocampi, Ser47-Akt (protein kinase B, PKB) phosphorylation increased from 4 h until 1 day post-injection (PI). Ser9-GSK3beta and Ser133-cAMP responsive element-binding protein (CREB) phosphorylations showed similar spatiotemporal patterns in hippocampi at 1 day until 3 days PI. Double immunohistochemistry also showed that these phosphorylated forms of Akt, GSK3beta and CREB were expressed in astrocytes. For the first time, our data demonstrate the injury-induced astrocytic changes in the levels of phosphorylation of Akt, -GSK3beta and -CREB in vivo, which may reflect mechanisms of glial cells protection or adaptive response to damage.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0364-3190
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1460-8
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Astrocytic expressions of phosphorylated Akt, GSK3beta and CREB following an excitotoxic lesion in the mouse hippocampus.
pubmed:affiliation
Department of Anatomy, Chungnam National University College of Medicine, Daejeon 301-131, South Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't