Seizure semiology, neurotransmitter receptors and cellular-stress responses in pentylenetetrazole models of epilepsy

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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 products and timely, research-based development of future therapeutic options. © 2012 Touch Group PLC.

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APA

Bidmon, H. J., Speckmann, E. J., & Zilles, K. J. (2009). Seizure semiology, neurotransmitter receptors and cellular-stress responses in pentylenetetrazole models of epilepsy. European Neurological Review, 4(1), 76–80. https://doi.org/10.17925/ENR.2009.04.01.76

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