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Interleukin-1β Alters Hebbian Synaptic Plasticity in Multiple Sclerosis.

Mario Stampanoni Bassi1, Fabio Buttari1, Carolina Gabri Nicoletti2

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|September 26, 2020
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Inflammation in multiple sclerosis (MS) disrupts brain plasticity. Elevated IL-1β levels in MS patients impair synaptic plasticity, leading to a loss of topographic specificity in motor pathways.

Keywords:
interleukin (IL)-1βlong-term potentiation (LTP)multiple sclerosis (MS)paired associative stimulation (PAS)synaptic plasticitytranscranial magnetic stimulation (TMS)

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Area of Science:

  • Neuroscience
  • Neuroimmunology
  • Neurophysiology

Background:

  • Inflammation significantly impacts synaptic transmission and plasticity in multiple sclerosis (MS).
  • The proinflammatory cytokine Interleukin-1 beta (IL-1β) is implicated in MS pathogenesis.
  • Understanding how IL-1β affects specific forms of synaptic plasticity is crucial for MS research.

Purpose of the Study:

  • To investigate the influence of IL-1β on Hebbian synaptic plasticity, specifically input specificity, in relapsing-remitting MS patients.
  • To examine the relationship between cerebrospinal fluid (CSF) IL-1β levels and synaptic plasticity measures.
  • To assess intracortical excitability and its association with IL-1β in MS.

Main Methods:

  • Paired associative stimulation (PAS) applied to the abductor pollicis brevis (APB) muscle in 33 MS patients and 15 healthy controls.
  • Assessment of motor-evoked potentials (MEPs) in APB and abductor digiti minimi (ADM) muscles post-PAS.
  • Measurement of intracortical excitability using paired-pulse transcranial magnetic stimulation (TMS) and quantification of CSF IL-1β levels.

Main Results:

  • MS patients showed impaired long-term potentiation (LTP)-like effects after PAS in the APB muscle.
  • A paradoxical increase in MEPs was observed in the ADM muscle of MS patients.
  • Higher IL-1β levels correlated negatively with LTP-like responses and were associated with increased synaptic hyperexcitability.

Conclusions:

  • IL-1β significantly disrupts Hebbian synaptic plasticity in MS, potentially causing a loss of topographic specificity.
  • Synaptic hyperexcitability, driven by IL-1β, may be a key mechanism underlying altered plasticity in MS.
  • These findings highlight the role of neuroinflammation in synaptic dysfunction in multiple sclerosis.