Immediate Early Gene Expression in Experimental Epilepsy

Immediate Early Gene Expression in Experimental Epilepsy Neuronal excitation by experimentally induced seizures elicits the rapid induction of a set of genes called immediate early genes (IEGs). The gene products of fos, jun and Krox, multimember gene families that belong to the class of IEGs, participate in a fundamental biological control mechanism, the regulation of gene transcription. IEG encoded proteins act as third messengers in an intracellular signal transduction cascade between neural cell surface receptors, cytoplasmic second messenger systems and specific target genes in the nucleus, a process for which the term ‘stimulus transcription coupling’ has been given. Almost all types of seizures cause dynamic alterations of IEG expression in neurons of the limbic system, but also in non‐limbic areas, such as the cortex, striatum and thalamus. IEG encoded transcription factors are thought to up‐ or down‐regulate effector genes with preferential expression in the central nervous system, including genes for neurotransmitters, growth factors, receptors, synaptic and axonal proteins. If the concept holds true that IEGs act as molecular switches converting epileptic short‐term excitation of neurons into alterations of the molecular phenotype, future research may help to explain hitherto unexplained phenomena in epileptogenesis including changes of synaptic efficacy, kindling and sprouting. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Pathology Wiley

Immediate Early Gene Expression in Experimental Epilepsy

Brain Pathology, Volume 3 (4) – Oct 1, 1993

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Publisher
Wiley
Copyright
Copyright © 1993 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1015-6305
eISSN
1750-3639
D.O.I.
10.1111/j.1750-3639.1993.tb00766.x
Publisher site
See Article on Publisher Site

Abstract

Neuronal excitation by experimentally induced seizures elicits the rapid induction of a set of genes called immediate early genes (IEGs). The gene products of fos, jun and Krox, multimember gene families that belong to the class of IEGs, participate in a fundamental biological control mechanism, the regulation of gene transcription. IEG encoded proteins act as third messengers in an intracellular signal transduction cascade between neural cell surface receptors, cytoplasmic second messenger systems and specific target genes in the nucleus, a process for which the term ‘stimulus transcription coupling’ has been given. Almost all types of seizures cause dynamic alterations of IEG expression in neurons of the limbic system, but also in non‐limbic areas, such as the cortex, striatum and thalamus. IEG encoded transcription factors are thought to up‐ or down‐regulate effector genes with preferential expression in the central nervous system, including genes for neurotransmitters, growth factors, receptors, synaptic and axonal proteins. If the concept holds true that IEGs act as molecular switches converting epileptic short‐term excitation of neurons into alterations of the molecular phenotype, future research may help to explain hitherto unexplained phenomena in epileptogenesis including changes of synaptic efficacy, kindling and sprouting.

Journal

Brain PathologyWiley

Published: Oct 1, 1993

References

  • Expression of c‐fos and c‐jun family genes after focal cerebral ischemia
    An, An; Lin, Lin; Liu, Liu; Xue, Xue; He, He; Hsu, Hsu
  • Enhanced rate of expression and biosynthesis of neuropeptide Y after kainic acid‐induced seizures
    Bellmann, Bellmann; Widmann, Widmann; Olenik, Olenik; Meyer, Meyer; Maas, Maas; Marksteiner, Marksteiner; Sperk, Sperk
  • Rapid rise in transcription factor mRNAs in rat brain after electroshock‐induced seizures
    Cole, Cole; Abu‐Shakra, Abu‐Shakra; Saffen, Saffen; Baraban, Baraban; Worley, Worley
  • Mouse brain c‐fos mRNA distribution following a single electroconvulsive shock
    Daval, Daval; Nakajima, Nakajima; Gleiter, Gleiter; Post, Post; Marangos, Marangos
  • Alterations of hippocampal acetylcholinesterase in human temporal lobe epilepsy
    Green, Green; Blume, Blume; Kupferschmid, Kupferschmid; Mesulam, Mesulam
  • Primary response genes induced by growth factors and tumor promoters
    Herschman, Herschman
  • Altered excitatory and inhibitory amino acid binding in hippocampus of patients with temporal lobe epilepsy
    McDonald, McDonald; Garofalo, Garofalo; Hood, Hood; Sackellares, Sackellares; Gilman, Gilman; McKeever, McKeever; Troncoso, Troncoso; Johnston, Johnston
  • Stimulus‐transcription coupling in the nervous system: Involvement of the inducible proto‐oncogenes fos and jun
    Morgan, Morgan; Curran, Curran
  • Fos‐like immunoreactivity induced by seizure in mice is specifically associated with euchromatin in neurons
    Mugnaini, Mugnaini; Berrebi, Berrebi; Morgan, Morgan; Curran, Curran
  • A selective loss of somatostatin in the hippocampus of patients with temporal lobe epilepsy
    Robbins, Robbins; Brines, Brines; Kim, Kim; Adrian, Adrian; Lanerolle, Lanerolle; Welsh, Welsh; Spencer, Spencer
  • 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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