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Minocycline attenuates microglial activation but fails to mitigate degeneration in inferior olive and pontine nuclei after focal cerebellar (Articolo in rivista)

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Minocycline attenuates microglial activation but fails to mitigate degeneration in inferior olive and pontine nuclei after focal cerebellar (Articolo in rivista) (literal)

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Viscomi M.T.1; Latini L.1; Florenzano F.1,2; Bernardi G.1,3; Molinari M.1,4 (2008)
Minocycline attenuates microglial activation but fails to mitigate degeneration in inferior olive and pontine nuclei after focal cerebellar
in Cerebellum (Lond., Print)
(literal)

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Viscomi M.T.1; Latini L.1; Florenzano F.1,2; Bernardi G.1,3; Molinari M.1,4 (literal)

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1 = Santa Lucia Foundation I.R.C.C.S., Via del Fosso di Fiorano 65, 00143 Rome, Italy; 2 = CNR INMM, Via del Fosso di Fiorano 65, 00143 Rome, Italy; 3 = Department of Neuroscience, University of Rome Tor Vergata, Viale Oxford 81, 00133 Rome, Italy; 4 = Experimental Neurorehabilitation Laboratory, Santa Lucia Foundation, Via Ardeatina 306, 00179 Rome, Italy (literal)

Titolo

Minocycline attenuates microglial activation but fails to mitigate degeneration in inferior olive and pontine nuclei after focal cerebellar (literal)

Abstract

Degenerative changes in areas remote from the primary lesion site have been linked to the clinical outcome of focal brain damage, and inflammatory mechanisms have been considered to play a key role in the pathogenesis of these remote cell death phenomena. Minocycline is a tetracycline derivative, therapeutically effective in various experimental models of central nervous system (CNS) injuries that include inflammatory and apoptotic mechanisms, although recent findings have yielded mixed results. In this study, we investigated the effectiveness of minocycline treatment in reducing remote cell death. Glial activation and neuronal loss in precerebellar stations following cerebellar lesion were investigated using immunohistochemistry and Western blot techniques. Our results show that minocycline was effective in reducing microglial activations in axotomized precerebellar nuclei, but failed to mitigate either astrocytic response or neuronal loss. This finding supports the role of minocycline in modulating inflammatory response after CNS lesion and suggests its ineffectiveness in influencing degenerative phenomena in areas remote from the primary lesion site. (literal)

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