Brain damage in a mouse model of global cerebral ischemia. Effect of NMDA receptor blockade.
(2003) In Brain Research 982(2). p.260-269- Abstract
- The importance of particular genes in neuronal death following global cerebral ischemia can readily be studied in genetically modified mice provided a reliable model of ischemia is available. For that purpose, we developed a mouse model of global cerebral ischemia that induces consistent damage to different regions of the brain and with a low mortality rate. Twelve minutes of ischemia was induced in C57BL/6 mice by bilateral common carotid artery occlusion under halothane anesthesia and artificial ventilation. Body and brain temperature were monitored and cortical cerebral blood flow in each hemisphere was measured by laser Doppler flowmeter before, during, and for 5 min after ischemia. Extensive damage was found in the striatum and marked... (More)
- The importance of particular genes in neuronal death following global cerebral ischemia can readily be studied in genetically modified mice provided a reliable model of ischemia is available. For that purpose, we developed a mouse model of global cerebral ischemia that induces consistent damage to different regions of the brain and with a low mortality rate. Twelve minutes of ischemia was induced in C57BL/6 mice by bilateral common carotid artery occlusion under halothane anesthesia and artificial ventilation. Body and brain temperature were monitored and cortical cerebral blood flow in each hemisphere was measured by laser Doppler flowmeter before, during, and for 5 min after ischemia. Extensive damage was found in the striatum and marked cell damage was observed in the CA1 and CA2 regions of hippocampus and in thalamus. Mild damage was seen in the CA3 region, dentate gyrus and cortex. Hippocampal damage in the CA1 region is delayed and developed over 48 h. Intraischemic hypothermia of 33 °C provided a robust neuroprotection. The non-competitive N-methyl-Image-aspartate receptor blocker, MK-801, did not provide protection in the hippocampus, cortex, striatum or thalamus when administered 30 min prior to ischemia or 2 h after the end of ischemia, but selectively mitigated damage in the hippocampus, when administered immediately following ischemia. This model of global cerebral ischemia may be useful in pharmacological and genomic studies of ischemic brain damage. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/117346
- author
- Olsson, Tomas ; Wieloch, Tadeusz LU and Smith, Maj-Lis LU
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Delayed neuronal death, Mouse, Hypothermia, Global ischemia, MK-801, Hippocampus
- in
- Brain Research
- volume
- 982
- issue
- 2
- pages
- 260 - 269
- publisher
- Elsevier
- external identifiers
-
- wos:000185316000012
- pmid:12915260
- scopus:0142057217
- ISSN
- 1872-6240
- DOI
- 10.1016/S0006-8993(03)03014-2
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Laboratory for Experimental Brain Research (013041000), Unit on Vascular Diabetic Complications (013241510)
- id
- 57896907-86cb-4ee0-ba11-8adb08c7c815 (old id 117346)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12915260&dopt=Abstract
- date added to LUP
- 2016-04-01 12:03:24
- date last changed
- 2022-01-26 22:07:27
@article{57896907-86cb-4ee0-ba11-8adb08c7c815,
abstract = {{The importance of particular genes in neuronal death following global cerebral ischemia can readily be studied in genetically modified mice provided a reliable model of ischemia is available. For that purpose, we developed a mouse model of global cerebral ischemia that induces consistent damage to different regions of the brain and with a low mortality rate. Twelve minutes of ischemia was induced in C57BL/6 mice by bilateral common carotid artery occlusion under halothane anesthesia and artificial ventilation. Body and brain temperature were monitored and cortical cerebral blood flow in each hemisphere was measured by laser Doppler flowmeter before, during, and for 5 min after ischemia. Extensive damage was found in the striatum and marked cell damage was observed in the CA1 and CA2 regions of hippocampus and in thalamus. Mild damage was seen in the CA3 region, dentate gyrus and cortex. Hippocampal damage in the CA1 region is delayed and developed over 48 h. Intraischemic hypothermia of 33 °C provided a robust neuroprotection. The non-competitive N-methyl-Image-aspartate receptor blocker, MK-801, did not provide protection in the hippocampus, cortex, striatum or thalamus when administered 30 min prior to ischemia or 2 h after the end of ischemia, but selectively mitigated damage in the hippocampus, when administered immediately following ischemia. This model of global cerebral ischemia may be useful in pharmacological and genomic studies of ischemic brain damage.}},
author = {{Olsson, Tomas and Wieloch, Tadeusz and Smith, Maj-Lis}},
issn = {{1872-6240}},
keywords = {{Delayed neuronal death; Mouse; Hypothermia; Global ischemia; MK-801; Hippocampus}},
language = {{eng}},
number = {{2}},
pages = {{260--269}},
publisher = {{Elsevier}},
series = {{Brain Research}},
title = {{Brain damage in a mouse model of global cerebral ischemia. Effect of NMDA receptor blockade.}},
url = {{http://dx.doi.org/10.1016/S0006-8993(03)03014-2}},
doi = {{10.1016/S0006-8993(03)03014-2}},
volume = {{982}},
year = {{2003}},
}