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Erratum: Persistent activation of microglia and NADPH oxidase drive hippocampal dysfunction in experimental multiple sclerosis (Scientific Reports (2016) 6 (20926) DOI: 10.1038/srep20926)

Authors :
Di Filippo, Massimiliano
De Iure, Antonio
Giampa', Carmela
Chiasserini, Davide
Tozzi, Alessandro
Orvietani, Pier Luigi
Ghiglieri, Veronica
Tantucci, Michela
Durante, Valentina
Quiroga Varela, Ana
Mancini, Andrea
Costa, Cinzia
Sarchielli, Paola
Fusco, Francesca Romana
Calabresi, Paolo
Giampa', Carmela (ORCID:0000-0001-8037-9214)
Calabresi, Paolo (ORCID:0000-0003-0326-5509)
Di Filippo, Massimiliano
De Iure, Antonio
Giampa', Carmela
Chiasserini, Davide
Tozzi, Alessandro
Orvietani, Pier Luigi
Ghiglieri, Veronica
Tantucci, Michela
Durante, Valentina
Quiroga Varela, Ana
Mancini, Andrea
Costa, Cinzia
Sarchielli, Paola
Fusco, Francesca Romana
Calabresi, Paolo
Giampa', Carmela (ORCID:0000-0001-8037-9214)
Calabresi, Paolo (ORCID:0000-0003-0326-5509)
Publication Year :
2016

Abstract

Cognitive impairment is common in multiple sclerosis (MS). Unfortunately, the synaptic and molecular mechanisms underlying MS-associated cognitive dysfunction are largely unknown. We explored the presence and the underlying mechanism of cognitive and synaptic hippocampal dysfunction during the remission phase of experimental MS. Experiments were performed in a chronic-relapsing experimental autoimmune encephalomyelitis (EAE) model of MS, after the resolution of motor deficits. Immunohistochemistry and patch-clamp recordings were performed in the CA1 hippocampal area. The hole-board was utilized as cognitive/behavioural test. In the remission phase of experimental MS, hippocampal microglial cells showed signs of activation, CA1 hippocampal synapses presented an impaired long-term potentiation (LTP) and an alteration of spatial tests became evident. The activation of hippocampal microglia mediated synaptic and cognitive/behavioural alterations during EAE. Specifically, LTP blockade was found to be caused by the reactive oxygen species (ROS)-producing enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. We suggest that in the remission phase of experimental MS microglia remains activated, causing synaptic dysfunctions mediated by NADPH oxidase. Inhibition of microglial activation and NADPH oxidase may represent a promising strategy to prevent neuroplasticity impairment associated with active neuro-inflammation, with the aim to improve cognition and counteract MS disease progression.

Details

Database :
OAIster
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1105026727
Document Type :
Electronic Resource