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Synaptic plasticity in multiple sclerosis and in experimental autoimmune encephalomyelitis

Robert Nisticò1, Francesco Mori, Marco Feligioni

  • 1Department of Physiology and Pharmacology, Sapienza University of Rome, , 00185 Rome, Italy.

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|December 4, 2013
PubMed

Insights

Multiple sclerosis (MS) patients often face cognitive issues. In a mouse model, enhanced IL-1β signaling in the hippocampus favors long-term potentiation, potentially explaining MS-related cognitive deficits.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Multiple sclerosis (MS) frequently causes cognitive dysfunction, impacting learning and memory.
  • Hippocampal pathology is implicated, but the precise mechanisms remain unclear.
  • Understanding synaptic changes in MS is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the mechanisms of cognitive deficits in a mouse model of MS.
  • To explore the role of interleukin-1 beta (IL-1β) in hippocampal synaptic function during experimental autoimmune encephalomyelitis (EAE).
  • To determine how altered synaptic plasticity contributes to MS-related cognitive impairment.

Main Methods:

  • Utilized the experimental autoimmune encephalomyelitis (EAE) mouse model to simulate MS.
  • Examined synaptic plasticity, specifically long-term potentiation (LTP) and long-term depression (LTD), in the hippocampus.
  • Assessed the role of IL-1β, lymphocytes, and microglia in modulating synaptic function.

Main Results:

  • In EAE mice, hippocampal LTP was favored over LTD following repetitive synaptic stimulation.
  • This shift in synaptic plasticity was dependent on enhanced IL-1β levels.
  • Elevated IL-1β originated from infiltrating lymphocytes and activated microglia.

Conclusions:

  • Pro-inflammatory cytokine IL-1β influences synaptic function and integrity in early MS.
  • Facilitated hippocampal LTP may contribute to both functional recovery and cognitive deficits in MS.
  • Targeting synaptic pathology, particularly IL-1β pathways, offers potential for new MS treatments.
Keywords:
experimental autoimmune encephalomyelitishippocampusinterleukin-1βlong-term potentiationmultiple sclerosissynaptic plasticity

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