Mouse hippocampal organotypic tissue cultures exposed to in vitro "ischemia" show selective and delayed CA1 damage that is aggravated by glucose
(2003) In Journal of Cerebral Blood Flow and Metabolism 23(1). p.23-33- Abstract
- Oxygen and glucose deprivation (OGD) in cell cultures is generally studied in a medium, such as artificial cerebrospinal fluid (CSF), with an ion composition similar to that of the extracellular fluid of the normal brain (2 to 4 mmol/L K+, 2 to 3 mmol/L Ca2+; pH 7.4). Because the distribution of ions across cell membranes dramatically shifts during ischemia, the authors exposed mouse organotypic hippocampal tissue cultures to OGD in a medium, an ischemic cerebrospinal fluid, with an ion composition similar to the extracellular fluid of the brain during ischemia in vivo (70 mmol/L K+, 0.3 mmol/L Ca2+; pH 6.8). In ischemic CSF, OGD induced a selective and delayed cell death in the CA1 region, as assessed by propidium iodide uptake. Cell... (More)
- Oxygen and glucose deprivation (OGD) in cell cultures is generally studied in a medium, such as artificial cerebrospinal fluid (CSF), with an ion composition similar to that of the extracellular fluid of the normal brain (2 to 4 mmol/L K+, 2 to 3 mmol/L Ca2+; pH 7.4). Because the distribution of ions across cell membranes dramatically shifts during ischemia, the authors exposed mouse organotypic hippocampal tissue cultures to OGD in a medium, an ischemic cerebrospinal fluid, with an ion composition similar to the extracellular fluid of the brain during ischemia in vivo (70 mmol/L K+, 0.3 mmol/L Ca2+; pH 6.8). In ischemic CSF, OGD induced a selective and delayed cell death in the CA1 region, as assessed by propidium iodide uptake. Cell death was glutamate receptor dependent since blockade of the N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors mitigated cell damage. Hyperglycemia aggravates ischemic brain damage in vivo, whereas in vitro glucose in artificial CSF prevents oxygen deprivation-induced damage. The authors demonstrate that glucose in ischemic CSF significantly exacerbates cell damage after oxygen deprivation. This new model of in vitro "ischemia" can be useful in future studies of the mechanisms and treatment of ischemic cell death, including studies using genetically modified mice. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/320655
- author
- Rytter, Anna LU ; Cronberg, Tobias LU ; Asztély, Fredrik LU ; Nemali, S and Wieloch, Tadeusz LU
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- anoxia, hyperglycemia, NMDA, brain ischemia, hippocampus, cell culture
- in
- Journal of Cerebral Blood Flow and Metabolism
- volume
- 23
- issue
- 1
- pages
- 23 - 33
- publisher
- Nature Publishing Group
- external identifiers
-
- wos:000180052000003
- pmid:12500088
- scopus:0037214462
- ISSN
- 1559-7016
- DOI
- 10.1097/00004647-200301000-00003
- language
- English
- LU publication?
- yes
- id
- dd5ff526-a20a-4b01-812a-7ef25a0ebd06 (old id 320655)
- date added to LUP
- 2016-04-01 15:36:21
- date last changed
- 2022-02-27 07:46:53
@article{dd5ff526-a20a-4b01-812a-7ef25a0ebd06, abstract = {{Oxygen and glucose deprivation (OGD) in cell cultures is generally studied in a medium, such as artificial cerebrospinal fluid (CSF), with an ion composition similar to that of the extracellular fluid of the normal brain (2 to 4 mmol/L K+, 2 to 3 mmol/L Ca2+; pH 7.4). Because the distribution of ions across cell membranes dramatically shifts during ischemia, the authors exposed mouse organotypic hippocampal tissue cultures to OGD in a medium, an ischemic cerebrospinal fluid, with an ion composition similar to the extracellular fluid of the brain during ischemia in vivo (70 mmol/L K+, 0.3 mmol/L Ca2+; pH 6.8). In ischemic CSF, OGD induced a selective and delayed cell death in the CA1 region, as assessed by propidium iodide uptake. Cell death was glutamate receptor dependent since blockade of the N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors mitigated cell damage. Hyperglycemia aggravates ischemic brain damage in vivo, whereas in vitro glucose in artificial CSF prevents oxygen deprivation-induced damage. The authors demonstrate that glucose in ischemic CSF significantly exacerbates cell damage after oxygen deprivation. This new model of in vitro "ischemia" can be useful in future studies of the mechanisms and treatment of ischemic cell death, including studies using genetically modified mice.}}, author = {{Rytter, Anna and Cronberg, Tobias and Asztély, Fredrik and Nemali, S and Wieloch, Tadeusz}}, issn = {{1559-7016}}, keywords = {{anoxia; hyperglycemia; NMDA; brain ischemia; hippocampus; cell culture}}, language = {{eng}}, number = {{1}}, pages = {{23--33}}, publisher = {{Nature Publishing Group}}, series = {{Journal of Cerebral Blood Flow and Metabolism}}, title = {{Mouse hippocampal organotypic tissue cultures exposed to in vitro "ischemia" show selective and delayed CA1 damage that is aggravated by glucose}}, url = {{http://dx.doi.org/10.1097/00004647-200301000-00003}}, doi = {{10.1097/00004647-200301000-00003}}, volume = {{23}}, year = {{2003}}, }