Multiple sclerosis (MS) is an inflammatory immune-mediate disorder of the central nervous system (CNS), primarily affecting the myelin sheath and followed by neurodegeneration. Synaptic alterations are emerging as critical determinants of early neurodegeneration in MS. Inflammation-induced alterations of synaptic transmission and plasticity have been investigated in vitro and also in human MS using transcranial magnetic stimulation (TMS) techniques. Specific inflammatory cytokines alter glutamatergic and GABAergic transmission, resulting in synaptic hyperexcitability. In both experimental autoimmune encephalomyelitis (EAE) and MS, excitotoxic damage and neurodegeneration are found even in the early phases of disease, conversely inflammation persists in the progressive phases. Inflammatory cytokines also affect synaptic plasticity, as both long-term potentiation (LTP) and long-term depression (LTD) are altered in EAE and in MS patients. In particular, inflammation profoundly subverts plasticity and influence both clinical recovery after a relapse and disease course. Regulation of neuronal activity by cytokines plays important roles in the neuro-immune crosstalk involved in inflammation-associated excitotoxic neuronal damage, and in the chance of developing compensatory plasticity. Innate and adaptive immunity interact with the CNS in MS, in line with the concept that cytokines and chemokines, in concert with neurotransmitters and neuropeptides, represent a major communication system in the CNS.

Stampanoni Bassi, M., Mori, F., Buttari, F., Marfia, G.a., Sancesario, A., Centonze, D., et al. (2017). Neurophysiology of synaptic functioning in multiple sclerosis. CLINICAL NEUROPHYSIOLOGY, 128(7), 1148-1157 [10.1016/j.clinph.2017.04.006].

Neurophysiology of synaptic functioning in multiple sclerosis

MORI, FRANCESCO;BUTTARI, FABIO;MARFIA, GIROLAMA ALESSANDRA;CENTONZE, DIEGO;
2017-07

Abstract

Multiple sclerosis (MS) is an inflammatory immune-mediate disorder of the central nervous system (CNS), primarily affecting the myelin sheath and followed by neurodegeneration. Synaptic alterations are emerging as critical determinants of early neurodegeneration in MS. Inflammation-induced alterations of synaptic transmission and plasticity have been investigated in vitro and also in human MS using transcranial magnetic stimulation (TMS) techniques. Specific inflammatory cytokines alter glutamatergic and GABAergic transmission, resulting in synaptic hyperexcitability. In both experimental autoimmune encephalomyelitis (EAE) and MS, excitotoxic damage and neurodegeneration are found even in the early phases of disease, conversely inflammation persists in the progressive phases. Inflammatory cytokines also affect synaptic plasticity, as both long-term potentiation (LTP) and long-term depression (LTD) are altered in EAE and in MS patients. In particular, inflammation profoundly subverts plasticity and influence both clinical recovery after a relapse and disease course. Regulation of neuronal activity by cytokines plays important roles in the neuro-immune crosstalk involved in inflammation-associated excitotoxic neuronal damage, and in the chance of developing compensatory plasticity. Innate and adaptive immunity interact with the CNS in MS, in line with the concept that cytokines and chemokines, in concert with neurotransmitters and neuropeptides, represent a major communication system in the CNS.
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/26 - Neurologia
English
Con Impact Factor ISI
Experimental autoimmune encephalomyelitis; Inflammatory cytokines; Multiple sclerosis; Neurodegeneration; Synaptic plasticity; Transcranial magnetic stimulation
The present study was funded by a grant from Fondazione Italiana Sclerosi Multipla (Progetto Speciale FISM, 2012/S/2), and by 5x1000 Neuromed grant to DC.
Stampanoni Bassi, M., Mori, F., Buttari, F., Marfia, G.a., Sancesario, A., Centonze, D., et al. (2017). Neurophysiology of synaptic functioning in multiple sclerosis. CLINICAL NEUROPHYSIOLOGY, 128(7), 1148-1157 [10.1016/j.clinph.2017.04.006].
Stampanoni Bassi, M; Mori, F; Buttari, F; Marfia, Ga; Sancesario, A; Centonze, D; Iezzi, E
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2108/185013
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