Selective c‐JUN Expression in CA1 Neurons of the Gerbil Hippocampus during and after Acquisition of an Ischemia‐Tolerant State

Selective c‐JUN Expression in CA1 Neurons of the Gerbil Hippocampus during and after... The selective delayed neuronal death of CA1 pyramidal cells after transient global ischemia in the gerbil brain can be prevented by preconditioning with a short sublethal period of ischemia 1–7 days prior to a subsequent, usually lethal ischemia of 5 min duration. Since changes of neuronal gene expression may play a crucial role in this tolerance induction, we investigated the postischemic expression profile of the fos, jun and Krox transcription factor families. We have previously reported that a single 5 min period of cerebral ischemia does not cause a de novo synthesis of immediate early gene (IEG) encoded proteins in CA1 neurons. In the present study, two experimental groups of Mongolian gerbils were investigated: one group was subjected to a single tolerance‐inducing 2.5 min period of ischemia by bilateral occlusion of the common carotid artery. The second (combined ischemia) group was subjected to 2.5 min of ischemia, followed by 5 min of ischemia 4 days later. Postischemic expression of c‐FOS, FOS B, c‐JUN, JUN B, JUN D and KROX‐24 was investigated by in situ hybridization and immunocytochemistry up to 48 h of recirculation. In contrast to a single 5 min period of ischemia, 2.5 min caused a postischemic expression of c‐JUN protein, but no other IEGs, in CA1 neurons (peak at 6 h). Similarly, a selective but delayed c‐JUN expression (peak at 18 h) was observed in animals subjected to combined ischemia. These results indicate that the induction of an endogenous neuroprotective state in CA1 neurons is associated with the activation of a genetic program which involves the expression of specific transcription factors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Pathology Wiley

Selective c‐JUN Expression in CA1 Neurons of the Gerbil Hippocampus during and after Acquisition of an Ischemia‐Tolerant State

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Publisher
Wiley
Copyright
Copyright © 1995 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1015-6305
eISSN
1750-3639
D.O.I.
10.1111/j.1750-3639.1995.tb00587.x
Publisher site
See Article on Publisher Site

Abstract

The selective delayed neuronal death of CA1 pyramidal cells after transient global ischemia in the gerbil brain can be prevented by preconditioning with a short sublethal period of ischemia 1–7 days prior to a subsequent, usually lethal ischemia of 5 min duration. Since changes of neuronal gene expression may play a crucial role in this tolerance induction, we investigated the postischemic expression profile of the fos, jun and Krox transcription factor families. We have previously reported that a single 5 min period of cerebral ischemia does not cause a de novo synthesis of immediate early gene (IEG) encoded proteins in CA1 neurons. In the present study, two experimental groups of Mongolian gerbils were investigated: one group was subjected to a single tolerance‐inducing 2.5 min period of ischemia by bilateral occlusion of the common carotid artery. The second (combined ischemia) group was subjected to 2.5 min of ischemia, followed by 5 min of ischemia 4 days later. Postischemic expression of c‐FOS, FOS B, c‐JUN, JUN B, JUN D and KROX‐24 was investigated by in situ hybridization and immunocytochemistry up to 48 h of recirculation. In contrast to a single 5 min period of ischemia, 2.5 min caused a postischemic expression of c‐JUN protein, but no other IEGs, in CA1 neurons (peak at 6 h). Similarly, a selective but delayed c‐JUN expression (peak at 18 h) was observed in animals subjected to combined ischemia. These results indicate that the induction of an endogenous neuroprotective state in CA1 neurons is associated with the activation of a genetic program which involves the expression of specific transcription factors.

Journal

Brain PathologyWiley

Published: Apr 1, 1995

References

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  • Induction of heat shock (stress) genes in the mammalian brain by hyperthermia and other traumatic events: a current perspective
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    Gass, Gass; Herdegen, Herdegen; Bravo, Bravo; Kiessling, Kiessling
  • Expression of c‐jun as a response to dorsal root and peripheral nerve section in damaged and adjacent intact primary sensory neurons in the rat
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  • Differential expression of immediate early genes in rubrospinal neurons following axotomy in rat
    Jenkins, Jenkins; Tetzlaff, Tetzlaff; Hunt, Hunt
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    Kiessling, Kiessling; Gass, Gass
  • The heat shock response
    Lindquist, Lindquist

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