Abstract
Structural and functional neuronal plasticity could play a crucial role during the course of multiple sclerosis (MS). The immune system and the central nervous system (CNS) strictly interact in physiologic conditions and during inflammation to modulate neuroplasticity and in particular the ability of the synapses to undergo long-term changes in the efficacy of synaptic transmission, such as long-term potentiation (LTP). During MS, neuro-inflammation might deeply influence the ability of neuronal networks to express physiologic plasticity, reducing the plastic reserve of the brain, with a negative impact on symptoms progression and cognitive performances. In this manuscript we review the evidence on synaptic plasticity alterations in experimental autoimmune encephalomyelitis (EAE), the most diffuse and widely utilized experimental model of MS, together with their potential underlying mechanisms and clinical relevance.
| Original language | English |
|---|---|
| Pages (from-to) | 205-213 |
| Number of pages | 9 |
| Journal | Brain Research |
| Volume | 1621 |
| DOIs | |
| Publication status | Published - Sep 24 2015 |
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Keywords
- EAE
- LTD
- LTP
- Multiple sclerosis
- Synaptic plasticity
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Neurology
- Developmental Biology
- Molecular Biology
Cite this
Synaptic plasticity and experimental autoimmune encephalomyelitis : Implications for multiple sclerosis. / Di Filippo, Massimiliano; De Iure, Antonio; Durante, Valentina; Gaetani, Lorenzo; Mancini, Andrea; Sarchielli, Paola; Calabresi, Paolo.
In: Brain Research, Vol. 1621, 24.09.2015, p. 205-213.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Synaptic plasticity and experimental autoimmune encephalomyelitis
T2 - Implications for multiple sclerosis
AU - Di Filippo, Massimiliano
AU - De Iure, Antonio
AU - Durante, Valentina
AU - Gaetani, Lorenzo
AU - Mancini, Andrea
AU - Sarchielli, Paola
AU - Calabresi, Paolo
PY - 2015/9/24
Y1 - 2015/9/24
N2 - Structural and functional neuronal plasticity could play a crucial role during the course of multiple sclerosis (MS). The immune system and the central nervous system (CNS) strictly interact in physiologic conditions and during inflammation to modulate neuroplasticity and in particular the ability of the synapses to undergo long-term changes in the efficacy of synaptic transmission, such as long-term potentiation (LTP). During MS, neuro-inflammation might deeply influence the ability of neuronal networks to express physiologic plasticity, reducing the plastic reserve of the brain, with a negative impact on symptoms progression and cognitive performances. In this manuscript we review the evidence on synaptic plasticity alterations in experimental autoimmune encephalomyelitis (EAE), the most diffuse and widely utilized experimental model of MS, together with their potential underlying mechanisms and clinical relevance.
AB - Structural and functional neuronal plasticity could play a crucial role during the course of multiple sclerosis (MS). The immune system and the central nervous system (CNS) strictly interact in physiologic conditions and during inflammation to modulate neuroplasticity and in particular the ability of the synapses to undergo long-term changes in the efficacy of synaptic transmission, such as long-term potentiation (LTP). During MS, neuro-inflammation might deeply influence the ability of neuronal networks to express physiologic plasticity, reducing the plastic reserve of the brain, with a negative impact on symptoms progression and cognitive performances. In this manuscript we review the evidence on synaptic plasticity alterations in experimental autoimmune encephalomyelitis (EAE), the most diffuse and widely utilized experimental model of MS, together with their potential underlying mechanisms and clinical relevance.
KW - EAE
KW - LTD
KW - LTP
KW - Multiple sclerosis
KW - Synaptic plasticity
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U2 - 10.1016/j.brainres.2014.12.004
DO - 10.1016/j.brainres.2014.12.004
M3 - Article
VL - 1621
SP - 205
EP - 213
JO - Brain Research
JF - Brain Research
SN - 0006-8993
ER -