Cited by 63Epilepsy research and treatmentProtease and Inhibitor MechanismsNeuroscience and Neuropharmacology Research

Matrix metalloproteinase-9 activity increased by two different types of epileptic seizures that do not induce neuronal death: A possible role in homeostatic synaptic plasticity

Takács, Eszter, Nyilas, Rita, Szepesi, Zsuzsanna, Baracskay, Péter, Karlsen, Bente, Røsvold, Tina, Bjørkum, Alvhild A., Czurkó, András +3 more·2010·Neurochemistry International

Abstract

Matrix metalloproteases (MMPs) degrade or modify extracellular matrix or membrane-bound proteins in the brain. MMP-2 and MMP-9 are activated by treatments that result in a sustained neuronal depolarization and are thought to contribute to neuronal death and structural remodeling. At the synapse, MMP actions on extracellular proteins contribute to changes in synaptic efficacy during learning paradigms. They are also activated during epileptic seizures, and MMP-9 has been associated with the establishment of aberrant synaptic connections after neuronal death induced by kainate treatment. It remains unclear whether MMPs are activated by epileptic activities that do not induce cell death. Here we examine this point in two animal models of epilepsy that do not involve extensive cell damage. We detected an elevation of MMP-9 enzymatic activity in cortical regions of secondary generalization after focal seizures induced by 4-aminopyridine (4-AP) application in rats. Pro-MMP-9 levels were also higher in Wistar Glaxo Rijswijk (WAG/Rij) rats, a genetic model of generalized absence epilepsy, than they were in Sprague-Dawley rats, and this elevation was correlated with diurnally occurring spike-wave-discharges in WAG/Rij rats. The increased enzymatic activity of MMP-9 in these two different epilepsy models is associated with synchronized neuronal activity that does not induce widespread cell death. In these epilepsy models MMP-9 induction may therefore be associated with functions such as homeostatic synaptic plasticity rather than neuronal death.

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Crossref · 10.1016/j.neuint.2010.03.003

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Authors
Takács, E., Nyilas, R., Szepesi, Z., Baracskay, P., Karlsen, B., Røsvold, T., Bjørkum, A. A., Czurkó, A., Kovács, Z., Kékesi, A. K., & Juhász, G.
Affiliations
  • Eötvös Loránd University (HU)
  • Høgskolen i Bergen (NO)
  • University of Sopron (HU)
Corresponding author
Takács, Eszter
Venue
Neurochemistry International
Publisher
Elsevier BV
Published
2010-05
Volume
56
Issue
6-7
Pages
799-809
ISSN
0197-0186 (ISSN-L)
OpenAlex
W1964178903
Cited by
63
References
103
Citations by year
2026: 2 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 4 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 7 · 2013: 3 · 2012: 8
FWCI
5.02
Type
journal article
Language
en
Open access
closed
Locations
  • Neurochemistry International (publishedVersion)
  • PubMed (publishedVersion)
Funders
Nemzeti Kutatási és Technológiai Hivatal
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
MMP-9, epileptic seizures, homeostatic plasticity, 4-aminopyridine-induced seizures, WAG/Rij rats, spike-wave discharges, secondary generalization, focal seizures, extracellular matrix remodeling, neuronal depolarization
MeSH terms
Animals, Behavior, Animal, Disease Models, Animal, Electroencephalography, Epilepsy, Frontal Lobe, Homeostasis, Male, Neuronal Plasticity, Neurons, Parietal Lobe, Synapses, Thalamus, 4-Aminopyridine, Cell Death, Rats, Sprague-Dawley, Rats, Wistar, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Potassium Channel Blockers, Rats

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