Alterations of Ca2+/calmodulin-dependent protein kinase II and its messenger RNA in the rat hippocampus following normo- and hypothermic ischemia
(1995) In Neuroscience 68(4). p.1003-1016- Abstract
The change in the subcellular distribution of Ca2+/calmodulin-dependent protein kinase II was studied in the rat hippocampus following normothermic and hypothermic transient cerebral ischemia of 15 min duration. A decrease in immunostaining of Ca2+/calmodulin-dependent protein kinase II was observed at 1 h of reperfusion which persisted until cell death in the CA1 region. In the CA3 and dentate gyrus areas immunostaining recovered at one to three days of reperfusion. The Ca2+/calmodulin-dependent protein kinase II was translocated to synaptic junctions during ischemia and reperfusion which could be due to a persistent change in the intracellular calcium ion homeostasis. The expression of the messenger... (More)
The change in the subcellular distribution of Ca2+/calmodulin-dependent protein kinase II was studied in the rat hippocampus following normothermic and hypothermic transient cerebral ischemia of 15 min duration. A decrease in immunostaining of Ca2+/calmodulin-dependent protein kinase II was observed at 1 h of reperfusion which persisted until cell death in the CA1 region. In the CA3 and dentate gyrus areas immunostaining recovered at one to three days of reperfusion. The Ca2+/calmodulin-dependent protein kinase II was translocated to synaptic junctions during ischemia and reperfusion which could be due to a persistent change in the intracellular calcium ion homeostasis. The expression of the messenger RNA of the α-subunit of Ca2+/calmodulin-dependent protein kinase II decreased in the entire hippocampus during reperfusion, and was most marked in the dentate gyrus at 12 h of reperfusion. This decrease could be a feedback downregulation of the mRNA due to increased Ca2+/calmodulin-dependent protein kinase II activation. Intraischemic hypothermia protected against ischemic neuronal damage and attenuated the ischemia-induced decrease of Ca2+/calmodulin-dependent protein kinase II immunostaining in all hippocampal regions. Hypothermia also reduced the translocation of Ca2+/calmodulin-dependent protein kinase II and restored Ca2+/calmodulin-dependent protein kinase II α messenger RNA after ischemia. The data suggest that ischemia leads to an aberrant Ca2+/calmodulin-dependent protein kinase II mediated signal transduction in the CA1 region, which is important for the delopment of delayed neuronal damage. Hypothermia enhances the restoration of the Ca2+/calmodulin-dependent protein kinase II mediated cell signalling.
(Less)
- author
- Hu, B. R. ; Kamme, F. LU and Wieloch, T. LU
- organization
- publishing date
- 1995-01-01
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Neuroscience
- volume
- 68
- issue
- 4
- pages
- 1003 - 1016
- publisher
- Elsevier
- external identifiers
-
- scopus:0028981464
- pmid:8544977
- ISSN
- 0306-4522
- DOI
- 10.1016/0306-4522(95)00213-3
- language
- English
- LU publication?
- yes
- id
- 5abb6716-4b49-4276-91e6-3b73246309db
- date added to LUP
- 2019-06-13 16:12:16
- date last changed
- 2024-01-01 10:13:52
@article{5abb6716-4b49-4276-91e6-3b73246309db,
abstract = {{<p>The change in the subcellular distribution of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II was studied in the rat hippocampus following normothermic and hypothermic transient cerebral ischemia of 15 min duration. A decrease in immunostaining of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II was observed at 1 h of reperfusion which persisted until cell death in the CA1 region. In the CA3 and dentate gyrus areas immunostaining recovered at one to three days of reperfusion. The Ca<sup>2+</sup>/calmodulin-dependent protein kinase II was translocated to synaptic junctions during ischemia and reperfusion which could be due to a persistent change in the intracellular calcium ion homeostasis. The expression of the messenger RNA of the α-subunit of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II decreased in the entire hippocampus during reperfusion, and was most marked in the dentate gyrus at 12 h of reperfusion. This decrease could be a feedback downregulation of the mRNA due to increased Ca<sup>2+</sup>/calmodulin-dependent protein kinase II activation. Intraischemic hypothermia protected against ischemic neuronal damage and attenuated the ischemia-induced decrease of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II immunostaining in all hippocampal regions. Hypothermia also reduced the translocation of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II and restored Ca<sup>2+</sup>/calmodulin-dependent protein kinase II α messenger RNA after ischemia. The data suggest that ischemia leads to an aberrant Ca<sup>2+</sup>/calmodulin-dependent protein kinase II mediated signal transduction in the CA1 region, which is important for the delopment of delayed neuronal damage. Hypothermia enhances the restoration of the Ca<sup>2+</sup>/calmodulin-dependent protein kinase II mediated cell signalling.</p>}},
author = {{Hu, B. R. and Kamme, F. and Wieloch, T.}},
issn = {{0306-4522}},
language = {{eng}},
month = {{01}},
number = {{4}},
pages = {{1003--1016}},
publisher = {{Elsevier}},
series = {{Neuroscience}},
title = {{Alterations of Ca2+/calmodulin-dependent protein kinase II and its messenger RNA in the rat hippocampus following normo- and hypothermic ischemia}},
url = {{http://dx.doi.org/10.1016/0306-4522(95)00213-3}},
doi = {{10.1016/0306-4522(95)00213-3}},
volume = {{68}},
year = {{1995}},
}