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Astrocytic Expressions of Phosphorylated Akt, GSK3β and CREB Following an Excitotoxic Lesion in the Mouse Hippocampus
| Content Provider | Semantic Scholar |
|---|---|
| Author | Kim, Dong Woon Lee, Jung Hoon Park, Sung Kyung Yang, Woo-Mi Jeon, Gye Sun Lee, Young Ho Chung, Chun Kee |
| Copyright Year | 2007 |
| Abstract | Glycogen synthase kinase 3β (GSK3β) 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 GSK3β, little is known about GSK3β changes in glial cells under neuropathological conditions. In this study, we evaluated the expressions of molecules associated with the GSK3β 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-GSK3β 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, GSK3β 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, -GSK3β and -CREB in vivo, which may reflect mechanisms of glial cells protection or adaptive response to damage. |
| Starting Page | 1460 |
| Ending Page | 1468 |
| Page Count | 9 |
| File Format | PDF HTM / HTML |
| DOI | 10.1007/s11064-007-9332-y |
| PubMed reference number | 17417726 |
| Journal | Medline |
| Volume Number | 32 |
| Alternate Webpage(s) | http://s-space.snu.ac.kr/bitstream/10371/13616/1/Kim-2007-Astrocytic%20expressio.pdf |
| Alternate Webpage(s) | https://doi.org/10.1007/s11064-007-9332-y |
| Journal | Neurochemical Research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
