Seizure Semiology, Neurotransmitter Receptors and Cellular-stress Responses in Pentylenetetrazole Models of Epilepsy

Seizure Semiology, Neurotransmitter Receptors and Cellular-stress Responses in Pentylenetetrazole Models of Epilepsy

Bidmon Hans-J, Speckmann Erwin-J, Zilles Karl J
European Neurological Review Volume 4 Issue 1
Published: November 2009
download article View ebook

| More
dots

Abstract
Ongoing research has elucidated a large variety of genes, proteins and enzyme products that are affected in epilepsy. Despite the pharmacological advances achieved by the development of antiepileptic drugs, numerous patients become pharmacoresistant. Therefore, animal models addressing these complex interactions among compensatory gene-expression cascades and consecutive molecular mechanisms are still a necessity for research-based gene and pharmacotherapy. In this article, we focus on pentylenetetrazole models to study the consequences of tonic–clonic seizures. We address two complex and closely linked aspects: alterations in neurotransmission and oxidative-stress responses. Reviewing just these two aspects highlights the need for a more standardised use of animal models and methods to allow a better integration of data from different lines of research. The latter will be most applicable for the understanding of complex disease-related interactions of gene networks, proteins and enzyme pr ducts and timely, research-based development of future therapeutic options.

Keywords
Epilepsy, gene networks, neurotransmission, cyclo-oxygenase, oxidative stress, neuron–glia interaction
Disclosure: The authors have no conflicts of interest to declare.
Received: 14 April 2009 Accepted: 15 July 2009
Correspondence: Hans-J Bidmon, C & O Vogt Institute for Brain Research, Heinrich-Heine-University, Düsseldorf, Bldg 22.03.05, University St 1, D-40225 Düsseldorf, Germany. E: hjb@hirn.uni-duesseldorf.de

Epilepsy affects about 1% of the human population at some point during their life. The causes of human epilepsies are diverse, ranging from defects during brain development resulting in dysplasias or ectopic cortical neurons to inherited forms involving certain mutations, e.g. ion channel defects or metabolic impairments; however, most causes are still unknown.1,2 Furthermore, posttraumatic epilepsies are also known;3 therefore, epilepsies are not a homogeneous pathogenetical entity, but rather are defined as the “occurrence of repeated seizures”,4 which will be grouped into various epileptic syndromes according to the individual semiology of patients.5

The causes of the initial mechanisms in the development of epileptic seizures are still elusive and only partial aspects of specific epileptic phenomena may be attributable to mutations at certain gene loci.6–8 Furthermore, during onset and progression of the disease, multiple changes in the expres ion patterns of many genes and gene products have been reported.2,9 This indicates that there are no single and specific gene mutations associated with a certain type of epilepsy, as has been established for Huntington’s disease, for example. These multiple molecular responses (at the level of genes, RNA splicing and proteins) provide strong evidence for the induction of pathology-associated responses.



To read full article please click here.

Keywords:
Epilepsy, gene networks, neurotransmission, cyclo-oxygenase, oxidative stress, neuron–glia interaction, Epilepsy symptoms, Epilepsy treatment, Epilepsy medication, cyclo-oxygenase 2, cyclo-oxygenase inhibitors, prostaglandin synthase, oxidative stress physiology, induced oxidative stress, oxidative stress response,

References:
  1. Lahl R, Villagran R, Teixeira W (eds), Neuropathology of focal epilepsies: An Atlas, Eastleigh, UK: John Libbey & Co., 2003.
  2. Lu Y, Wang X, Neurol Res, 2009;31:135–43.
  3. Pitkänen A, Immonen RJ, Gröhn OH, et al., Epilepsia, 2009;(50 Suppl. 2):21–9.
  4. Fish DR. In: Scaravilli F (ed.), Neuropathology of Epilepsy, Singapore: World Scientific Publ. Co., 1998;11–43.
  5. Commission on Classification and Terminology of the International League Against Epilepsy, Epilepsia, 1989;30:389–99.
  6. Benarroch EE, Neurology, 2009;72:664–9.
  7. Gargus JJ, Ann N Y Acad Sci, 2009;1151:133–56.
  8. Mullen SA, Scheffer IE, Arch Neurol, 2009;66:21–6.
  9. Majak K, Dabrowski M, Pitkänen A, Neurosience, 2009;159: 468–82.
  10. Kuteykin-Teplyakov K, Brandt C, Hoffmann K, et al., Epilepsia, 2009;50(4):887–97.
  11. Jefferys JGR, Traub RD. In: Scaravilli F (ed.), Neuropathology of Epipilepsy, Singapore: World Scientific Publ Co, 1997;45–76.
  12. White HS, Neurology, 2002;59:S7–S14.
  13. Macdonald RL, Barker JL, Neurology, 1978;28:325 –30.
  14. Huang RQ, Bell-Horner CL, Dibas ML, et al., J Pharmacol Exp Ther, 2001;298:986–95.
  15. Jonker DM, Voskuyl RA, Danhof M, Epilepsia, 2007;48:412–34.
  16. Kato K, Katoh-Semba R, Takeuchi IK, et al., J Neurochem, 1999;73:229–36.
  17. He DF, Ma DL, Tang YC, et al., Brain Pathol, 2009.
  18. Speckmann E-J (ed.), Experimentelle Epilepsieforschung Wissenschaftliche Buchgesellschaft, Darmstadt, 1986.
  19. Speckmann E-J, Elger CE. In: Niedermeyer E, Lopes Da Silva F (eds), Electroencephalography: Basic Principles, Clinical Applications, and Related Fields, Baltimore-München: Urban & Schwarzenberg, 1998;15–27.
  20. Speckmann E-J, Elger CE, Altrup U. In: Wyllie E (ed.), The Treatment of Epilepsy: Principles & Practice, Philadelphia– Baltimore–New York–London–Buenos Aires–Hong Kong–Sydney–Tokyo: Lippincott Williams & Wilkins, 2001;149–63.
  21. Bidmon HJ, Görg B, Palomero-Gallagher N, et al., J Chem Neuroanat, 2005;30:1–16.
  22. Tchekalarova J, Sotiriou E, Georgiev V, et al., Brain Res, 2005; 1032(1–2):94–103.
  23. Angelatou F, Pagonopoulou O, Kostopoulos G, Neurosci Lett, 2003;132:203–6.
  24. Angelatou F, Pagonopoulou O, Kostopoulos G, Brain Res, 1990;534: 251–6.
  25. Ekonomou A, Sperk G, Kostopoulos G, et al., Neurosci Lett, 2000;284:49–52.
  26. Cremer CM, Palomero-Gallagher N, Bidmon HJ, et al., Neuroscience, 2009.
  27. Ekonomou A, Smith AL, Angelatou F, Brain Res Mol Brain Res, 2001;95:27–35.
  28. Ekonomou A, Angelatou F, Neurochem Res,1999;24: 1515–22.
  29. Gmiro VE, Serdyuk SE, Bull Exp Biol Med, 2008;145: 728–30.
  30. Luthman J, Humpel C, Neurosci Lett, 1997;239:9–12.
  31. Tchekalarova J, Sotiriou E, Angelatou F, Brain Res, 2004;1024:159–66.
  32. Szyndler J, Rok P, Maciejak P, et al., Pharmacol Biochem Behav, 2002;73:851–61.
  33. Weinshenker D, Szot P, Miller NS, et al., J Pharmacol Exp Ther, 2001;298:1042–8.
  34. Caspers H, Speckmann EJ, Epilepsia, 1972;13: 699–725.
  35. Patsoukis N, Zervoudakis G, Georgiou CD, et al., Epilepsia, 2005;46:1205–11.
  36. Patsoukis N, Zervoudakis G, Georgiou CD, et al., Epilepsy Res, 2004;62: 65–74.
  37. Patsoukis N, Zervoudakis G, Panagopoulos NT, et al., Neurosci Lett, 2004;357:83–6.
  38. Rauca C, Wiswedel I, Zerbe R, et al., Brain Res, 2004;1009:203–12.
  39. Bashkatova V, Narkevich V, Vitskova G, et al., Prog Neuropsychopharmacol Biol Psychiatry, 2003;27:487–92.
  40. Bidmon HJ, Görg B, Palomero-Gallagher N, et al., Epilepsia, 2008;49: 1733–8.
  41. Itoh K, Watanabe M, Neuroscience, 2009;159:735–43.
  42. Yermakova A, O’Banion MK, Curr Pharmaceutical Design, 2000;6: 1755–76.
  43. Oliveira M S, Furian AF, Rambo LM, et al., Neuroscience, 2008;152:1110–18.
  44. Oliveira MS, Furian AF, Rambo LM, et al., J Neurochem, 2009;109(2):416–26.
  45. Bidmon H-J, Oermann E, Schiene K, et al., J Chem Neuroanat, 2000;20:163–76.
  46. Bidmon H-J, Emde B, Kowalski T, et al., J Chem Neuroanat, 2001;22:167–84.
  47. Bidmon H-J, Palomero-Gallagher N, Zilles K, Clin Neurophysiol, 2002;32:163–77.
  48. Oermann E, Bidmon H-J, Mayer B, et al., Anat Embryol, 200:27–41.
  49. Bidmon H-J, Wu J, Gödecke A, et al., Neuroscience, 1997;81:321–30.
  50. Freichel C, Potschka H, Ebert U, et al., Neuroscience, 2006;141: 2177–94.
  51. Motte JE, da Silva Fernandes MJ, Marescaux C, et al., Brain Res Mol Brain Res, 1997;50:79–84.
  52. Ammon-Treiber S, Grecksch G, Angelidis C, et al., Naunyn Schmiedebergs Arch Pharmacol, 2007;375:115–21.
  53. Hertz L, Zielke HR, Trends Neurosci, 2004;27:735–43.
  54. Tian GF, Azmi H, Takano T, et al., Nat Medicine, 2005;11:973–81.
  55. Löscher W, Gernert M, Heinemann U, Trends Neurosci, 2008;31:62–73.

Copyright® 2004 - 2010 Business Briefings, Ltd. All rights reserved.
Touch Neurology is for informational purposes and should not be considered medical advice, diagnosis or treatement recommendations.