Induction of junD mRNA after transient forebrain ischemia in the rat. Effect of hypothermia
(1996) In Molecular Brain Research 43(1-2). p.51-56- Abstract
The expression of junD was studied in the rat hippocampus by in situ hybridization after 15 min of normothermic (37°C) and hypothermic (33°C) transient forebrain ischemia. Ischemia was induced by common carotid artery occlusion combined with hypotension leading to damage in the CA1 region of the hippocampus which was prevented by hypothermia junD mRNA was induced in the hippocampus within 2 h of reperfusion and was strong in the dentate gyrus but weak in the CA3 acid CA1 subregions. Intraischemic hypothermia significantly augmented the junD induction in the dentate gyrus. During late reperfusion (between 12 and 36 h after ischemia) a transient increase in junD mRNA was seen in the normothernic CA3 which was abolished in the hypothermic... (More)
The expression of junD was studied in the rat hippocampus by in situ hybridization after 15 min of normothermic (37°C) and hypothermic (33°C) transient forebrain ischemia. Ischemia was induced by common carotid artery occlusion combined with hypotension leading to damage in the CA1 region of the hippocampus which was prevented by hypothermia junD mRNA was induced in the hippocampus within 2 h of reperfusion and was strong in the dentate gyrus but weak in the CA3 acid CA1 subregions. Intraischemic hypothermia significantly augmented the junD induction in the dentate gyrus. During late reperfusion (between 12 and 36 h after ischemia) a transient increase in junD mRNA was seen in the normothernic CA3 which was abolished in the hypothermic brains. In contrast, in the normothermic CA1 a continuous increase of junD was seen. This was significantly reduced by intraischemic hypothermia. We suggest that the early induction in junD expression in the dentate gyrus and in the hypothermic CA3 region is a protective reaction to the ischemic stress. The marked increase in resistant brain areas could be due to the preserved intracellular signaling pathways and a subsequent maintenance of protein synthesis. The late continuous increase, unique to the vulnerable normothermic CA1 region, suggests that junD participates in a transcriptional process that may be important for delayed neuronal death in the hippocampus following transient forebrain ischemia.
(Less)
- author
- Kamme, Fredrik LU and Wieloch, Tadeusz LU
- organization
- publishing date
- 1996-12-31
- type
- Contribution to journal
- publication status
- published
- keywords
- Hippocampus, Immediate early gene, In situ hybridization, Neuronal death, Signal transduction
- in
- Molecular Brain Research
- volume
- 43
- issue
- 1-2
- pages
- 51 - 56
- publisher
- Elsevier
- external identifiers
-
- pmid:9037518
- scopus:0030608447
- ISSN
- 0169-328X
- DOI
- 10.1016/S0169-328X(96)00151-9
- language
- English
- LU publication?
- yes
- id
- ba389d18-7259-4254-b791-2a87d4cae733
- date added to LUP
- 2016-10-05 16:10:24
- date last changed
- 2024-03-22 09:07:13
@article{ba389d18-7259-4254-b791-2a87d4cae733,
abstract = {{<p>The expression of junD was studied in the rat hippocampus by in situ hybridization after 15 min of normothermic (37°C) and hypothermic (33°C) transient forebrain ischemia. Ischemia was induced by common carotid artery occlusion combined with hypotension leading to damage in the CA1 region of the hippocampus which was prevented by hypothermia junD mRNA was induced in the hippocampus within 2 h of reperfusion and was strong in the dentate gyrus but weak in the CA3 acid CA1 subregions. Intraischemic hypothermia significantly augmented the junD induction in the dentate gyrus. During late reperfusion (between 12 and 36 h after ischemia) a transient increase in junD mRNA was seen in the normothernic CA3 which was abolished in the hypothermic brains. In contrast, in the normothermic CA1 a continuous increase of junD was seen. This was significantly reduced by intraischemic hypothermia. We suggest that the early induction in junD expression in the dentate gyrus and in the hypothermic CA3 region is a protective reaction to the ischemic stress. The marked increase in resistant brain areas could be due to the preserved intracellular signaling pathways and a subsequent maintenance of protein synthesis. The late continuous increase, unique to the vulnerable normothermic CA1 region, suggests that junD participates in a transcriptional process that may be important for delayed neuronal death in the hippocampus following transient forebrain ischemia.</p>}},
author = {{Kamme, Fredrik and Wieloch, Tadeusz}},
issn = {{0169-328X}},
keywords = {{Hippocampus; Immediate early gene; In situ hybridization; Neuronal death; Signal transduction}},
language = {{eng}},
month = {{12}},
number = {{1-2}},
pages = {{51--56}},
publisher = {{Elsevier}},
series = {{Molecular Brain Research}},
title = {{Induction of junD mRNA after transient forebrain ischemia in the rat. Effect of hypothermia}},
url = {{http://dx.doi.org/10.1016/S0169-328X(96)00151-9}},
doi = {{10.1016/S0169-328X(96)00151-9}},
volume = {{43}},
year = {{1996}},
}