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SP protects cerebellar granule cells against beta-amyloid-induced apoptosis by down-regulation and reduced activity of Kv4 potassium channels (Articolo in rivista)

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SP protects cerebellar granule cells against beta-amyloid-induced apoptosis by down-regulation and reduced activity of Kv4 potassium channels (Articolo in rivista) (literal)

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M. Pieri b, c; G. Amadoro a; I. Carunchio b, c; M.T. Ciotti a; S. Quaresima a; F. Florenzano a, d; P. Calissano a, b, e; R. Possenti a, b; C. Zona b, c; C.Severini a (2010)
SP protects cerebellar granule cells against beta-amyloid-induced apoptosis by down-regulation and reduced activity of Kv4 potassium channels
in Neuropharmacology
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

M. Pieri b, c; G. Amadoro a; I. Carunchio b, c; M.T. Ciotti a; S. Quaresima a; F. Florenzano a, d; P. Calissano a, b, e; R. Possenti a, b; C. Zona b, c; C.Severini a (literal)

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a Institute of Neurobiology and Molecular Medicine, CNR, Via del Fosso di Fiorano, 65, 00143 Rome, Italy b Department of Neuroscience, University of Rome \"Tor Vergata\", Via Montpellier, 1, 00133, Rome, Italy c C.E.R.C. Fondazione S. Lucia, Via del Fosso di Fiorano, 65, 00143 Rome, Italy d Confocal Microscopy Unit, EBRI-CNR-Fondazione S. Lucia, Via del Fosso di Fiorano, 65, 00143 Rome, Italy e European Brain Research Institute, Via del Fosso di Fiorano, 65, 00143 Rome, Italy (literal)

Titolo

SP protects cerebellar granule cells against beta-amyloid-induced apoptosis by down-regulation and reduced activity of Kv4 potassium channels (literal)

Abstract

The tachykinin endecapeptide substance P (SP) has been demonstrated to exert a functional role in neurodegenerative disorders, including Alzheimer's disease (AD). Aim of the present study was to evaluate the SP neuroprotective potential against apoptosis induced by the neurotoxic beta-amyloid peptide (A beta) in cultured rat cerebellar granule cells (CGCs). We found that SP protects CGCs against both A beta(25-35)- and A beta(1-42)-induced apoptotic CGCs death as revealed by live/dead cell assay, Hoechst staining and caspase(s)-induced PARP-1 cleavage, through an Akt-dependent mechanism. Since in CGCs the fast inactivating or A-type K(+) current (I(KA)) was potentiated by A beta treatment through up-regulation of Kv4 subunits, we investigated whether I(KA) and the related potassium channel subunits could be involved in the SP anti-apoptotic activity. Patch-clamp experiments showed that the A beta-induced increase of I(KA) current amplitude was reversed by SP treatment. In addition, as revealed by Western blot analysis and immunofluorescence studies, SP prevented the up-regulation of Kv4.2 and Kv4.3 channel subunits expression. These results indicate that SP plays a role in the regulation of voltage-gated potassium channels in A beta-mediated neuronal death and may represent a new approach in the understanding and treatment of AD. (literal)

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