4.7 Article

Anti-inflammatory cytokines, TGF-β1 and IL-10, exert anti-hypoxic action and abolish posthypoxic hyperexcitability in hippocampal slice neurons: Comparative aspects

Journal

EXPERIMENTAL NEUROLOGY
Volume 232, Issue 2, Pages 329-332

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2011.09.004

Keywords

Hippocampal slice; Hypoxia; Interleukin-10; Transforming growth factor-beta; Population spike; Posthypoxic hyperexcitability; Hypoxic preconditioning

Categories

Funding

  1. Russian Ministry of High Education and Science [2.1.1 / 11499, Pi610]

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The aim of this study was to investigate the comparative effects of transforming growth factor beta 1 (TGF-beta 1) and interleukin-10 (IL-10) on the repeated brief hypoxia-induced alterations in the activity of hippocampal slice CA1 pyramidal neurons. The method of field potentials measurement in CA1 region of hippocampal slices was used. The principal results of our work are summarized as follow. 1. TGF-beta 1 reduces the depressive effect of brief hypoxia on the population spike amplitude more effectively than IL-10. 2. During TGF-beta 1 exposure (in contrast to IL-10), three 3-min hypoxic episodes do not induce the rapid hypoxic preconditioning. 3. TGF-beta 1 and IL-10 equally abolish posthypoxic hyperexcitability induced by repeated brief episodes of hypoxia in CA1 pyramidal neurons. These findings indicated that TGF-beta 1 and IL-10 are able to evoke anti-hypoxic effect and abolish the development of posthypoxic hyperexcitability induced by repeated brief hypoxic episodes in hippocampal CA1 pyramidal neurons. Our results also demonstrated that TGF-beta 1 reduced the effectiveness of hypoxia to depress neuronal activity more effectively than IL-10. We suggest that the present findings allow to explain the certain neuroprotective mechanisms of IL-10 and TGF-beta1 in the early phase of hypoxia and indicate that a therapeutic anti-inflammatory approach using these substances can provide neuroprotection in the brain hypoxic conditions. (C) 2011 Elsevier Inc. All rights reserved.

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