Dynamic Changes in the Composition of the AP‐1 Transcription Factor DNA‐binding Activity in Rat Brain Following Kainate‐induced Seizures and Cell Death

Dynamic Changes in the Composition of the AP‐1 Transcription Factor DNA‐binding Activity in... Kainate, a potent excitatory and neurotoxic agent, has also proved useful in studies on other glutamate‐driven phenomena, such as neuronal plasticity. Long‐term effects of kainate are apparently dependent on its influence on the expression of various genes, including those encoding the AP‐1 transcription factor, consisting of proteins belonging to the Fos and Jun families. In our studies we analysed c‐fos, fos B, c‐jun, jun B and jun D mRNA levels as well as a functional feature of AP‐1, its DNA‐binding activity, in the rat brain following systemic injection of kainate. Two phases of elevated AP‐1 DNA‐binding activity were observed in the hippocampus and entorhinal cortex, and were correlated with period of seizures (2 and 6 h after kainate injection) and neuron damage (48–72 h). At 72 h after kainate treatment DNA fragmentation, believed to be diagnostic of apoptotic processes typical of programmed cell death phenomena, was noted. Two and six hours after the treatment, AP‐1 consisted predominantly of Fos B, c‐Fos, Fra‐2 and Jun B, while at 72 h Jun D constituted the major AP‐1 component in place of Jun B, and no c‐Fos was detected. Only a slight AP‐1 increase was seen 24 h after kainate treatment. In the sensory cortex, only the late phase of AP‐1 elevation was detected. Contrary to AP‐1, no effect of kainate on levels of two other transcription factors, CREB/ATF (cAMP‐responsive element binding proteins) and OCT (octamer element DNA‐binding activity) was seen. However, the level of OCT DNA‐binding activity was higher in the sensory cortex than in other two structures examined. These data point to a selective effect of kainate on AP‐1 in brain structures known to be particularly vulnerable to kainate, and suggest a role of AP‐1 transcription factor, and more selectively Jun D protein, in kainate‐driven programmed neuronal death. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

Dynamic Changes in the Composition of the AP‐1 Transcription Factor DNA‐binding Activity in Rat Brain Following Kainate‐induced Seizures and Cell Death

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Publisher
Wiley
Copyright
Copyright © 1994 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0953-816X
eISSN
1460-9568
D.O.I.
10.1111/j.1460-9568.1994.tb00546.x
Publisher site
See Article on Publisher Site

Abstract

Kainate, a potent excitatory and neurotoxic agent, has also proved useful in studies on other glutamate‐driven phenomena, such as neuronal plasticity. Long‐term effects of kainate are apparently dependent on its influence on the expression of various genes, including those encoding the AP‐1 transcription factor, consisting of proteins belonging to the Fos and Jun families. In our studies we analysed c‐fos, fos B, c‐jun, jun B and jun D mRNA levels as well as a functional feature of AP‐1, its DNA‐binding activity, in the rat brain following systemic injection of kainate. Two phases of elevated AP‐1 DNA‐binding activity were observed in the hippocampus and entorhinal cortex, and were correlated with period of seizures (2 and 6 h after kainate injection) and neuron damage (48–72 h). At 72 h after kainate treatment DNA fragmentation, believed to be diagnostic of apoptotic processes typical of programmed cell death phenomena, was noted. Two and six hours after the treatment, AP‐1 consisted predominantly of Fos B, c‐Fos, Fra‐2 and Jun B, while at 72 h Jun D constituted the major AP‐1 component in place of Jun B, and no c‐Fos was detected. Only a slight AP‐1 increase was seen 24 h after kainate treatment. In the sensory cortex, only the late phase of AP‐1 elevation was detected. Contrary to AP‐1, no effect of kainate on levels of two other transcription factors, CREB/ATF (cAMP‐responsive element binding proteins) and OCT (octamer element DNA‐binding activity) was seen. However, the level of OCT DNA‐binding activity was higher in the sensory cortex than in other two structures examined. These data point to a selective effect of kainate on AP‐1 in brain structures known to be particularly vulnerable to kainate, and suggest a role of AP‐1 transcription factor, and more selectively Jun D protein, in kainate‐driven programmed neuronal death.

Journal

European Journal of NeuroscienceWiley

Published: Oct 1, 1994

References

  • Spatiotemporal induction of immediate early genes in the rat brain after limbic seizures: effects of NMDA receptor antagonist MK‐801
    Gass, Gass; Herdegen, Herdegen; Bravo, Bravo; Kiessling, Kiessling
  • Molecular biology of vertebrate learning: is c‐fos a new beginning
    Kaczmarek, Kaczmarek
  • Stimulus‐transcription coupling in the nervous system: involvement of the inducible proto‐oncogenes fos and jun
    Morgan, Morgan; Curran, Curran
  • Immunohistochemistry of c‐fos in mouse brain during postnatal development: basal levels and changing response to metrazol and kainate injection
    Sakurai‐Yamashita, Sakurai‐Yamashita; Sassone‐Corsi, Sassone‐Corsi; Gombos, Gombos
  • Glutamate receptor agonists increase the expression of Fos, Fra and AP‐1 DNA binding activity in the mammalian brain
    Sonnenberg, Sonnenberg; Mitchelmore, Mitchelmore; Macgregor‐Leon, Macgregor‐Leon; Hempstead, Hempstead; Morgan, Morgan; Curran, Curran

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