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2017 | 77 | Suppl.1 |
Tytuł artykułu

MMP-9 activity in animal model of traumatic brain injury

Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
INTRODUCTION: Epilepsy in 20% of cases, develops as an effect of traumatic brain injury (TBI). Recent evidences indicate important role of extracellular matrix metalloproteinase-9 (MMP-9) in neuronal circuitry remodeling and synaptic plasticity. AIM(S): The aim of the present study was to evaluate the MMP-9 activity changes, dendritic spines density after brain injury and the influence of MMP‑9 expression level on spontaneous seizures appearance after TBI. METHOD(S): We used Controlled Cortical Impact (CCI) as a model of TBI in animals with altered MMP-9 levels (lacking: MMP-9 KO; overexpressing: MMP-9 OE) and their WT siblings. 12 weeks after CCI animals were subjected to continuous video-EEG monitoring. To verify MMP-9 changes after TBI: gel zymography and in situ hybridization were used. For dendritic spine alterations staining using liophilic dye DiI were performed. RESULTS: TBI resulted in progressive cortex (Cx) degeneration during 30 days after TBI. This effect was MMP-9 dependent. In MMP-9 KO animals degeneration volume degree was significantly smaller compared to wildtype siblings and MMP-9 OE mice. Gel zymography analysis showed time-associated elevation of MMP-9 activity in ipsilateral Cx and Hp, also in the thalamus samples during 3 days after CCI. Moreover, in situ hybridization showed increase of MMP-9 mRNA expression which reached the peak 6 hours post-CCI. Density of the dendritic spines measured 7 and 14 d after CCI was significantly decreased in ipsilateral Cx and CA1. EEG recordings with threshold test showed decreased seizure latency in MMP-9 OE mice while increased in MMP-9 KO. Interestingly total seizure number was the highest in MMP-9 OE animals. CONCLUSIONS: We described the correlation between TBI and MMP-9 activity and action post trauma. We indicated that MMP-9 might be an important factor for major dendritic spine reshaping, observed after brain injury, which in consequence may lead to altered sensibility of neuronal circuits to trigger seizures. FINANCIAL SUPPORT: This work was supported by PBS Program founded by The National Centre of Research and Development.
Słowa kluczowe
Wydawca
-
Rocznik
Tom
77
Numer
Opis fizyczny
p.55-56
Twórcy
autor
  • Department of Molecular and Cellular Neurobiology, Laboratory of Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
  • Department of Molecular and Cellular Neurobiology, Laboratory of Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
  • Department of Molecular and Cellular Neurobiology, Laboratory of Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
autor
  • Department of Molecular and Cellular Neurobiology, Laboratory of Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland
Bibliografia
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.agro-e4aa8713-e73b-439d-add5-1f4ac61a6f46
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