Attenuation of inflammatory response after stroke allows to retain brain plasticity

• Autorzy: Liguz-Lecznar M. , Jablonka J. , Kossut M.
• Języki publikacji: EN

Abstrakty

EN

Despite indications that brain plasticity may be enhanced after stroke, we have described impairment of experience-dependent plasticity in rodent cerebral cortex neighbouring the stroke-induced lesion. There is increasing evidence showing that inflammation accounts for stroke progression. Once activated, inflammatory cells can release a variety of cytotoxic agents that may induce more cell damage as well as disruption of the blood-brain barrier and extracellular matrix. We have shown that chronic treatment with anti-inflammatory drug ibuprofen restored plasticity of cortical representation of vibrissae induced by whisker deprivation. We have also the upregulation cyclooxygenase-2 (COX-2) and other proinflammatory factors, i.e. IL-1 and tumor necrosis factor TNFα shown in the acute poststroke phase. Since TNFα is one of the key players in stroke progression, we decided to reduce the TNFα signalling by introduction into the brain soluble TNFα receptors 1 that will compete for TNFα with receptors localized in the brain tissue. We have shown that such approach undertaken simultaneously with the stroke was successful in preserving the poststroke brain plasticity. Supported by Polish National Science Centre Grant: N N401 098739.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2013
• Tom: 73
• Numer: Suppl.1
• Opis fizyczny: p.22

Twórcy

autor

Liguz-Lecznar M.

• Department of Cellular and Molecular Biology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland

autor

Jablonka J.

• Department of Neurophysiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland

autor

Kossut M.

• Department of Cellular and Molecular Biology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland