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Related Experiment Video

Updated: May 7, 2026

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
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Cladribine interferes with IL-1β synaptic effects in experimental multiple sclerosis.

Alessandra Musella1, Georgia Mandolesi, Antonietta Gentile

  • 1Fondazione Santa Lucia, Centro Europeo per la Ricerca sul Cervello (CERC), 00143 Rome, Italy; UOC Neurologia, Dipartimento di Medicina dei Sistemi, Università Tor Vergata, 00133 Rome, Italy.

Journal of Neuroimmunology
|September 19, 2013
PubMed
Summary

Cladribine, delivered intracerebroventricularly, reduced multiple sclerosis (MS) symptoms in mice by protecting against synaptic damage. This neuroprotection occurred independently of its immunosuppressive effects.

Keywords:
CladribineEAEEPSCIL-1βMicrogliaStriatum

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Area of Science:

  • Neuroimmunology
  • Neuropharmacology
  • Neurophysiology

Background:

  • Multiple sclerosis (MS) involves glutamate-mediated synaptic transmission alterations.
  • Experimental autoimmune encephalomyelitis (EAE) models MS, exhibiting similar synaptic dysfunction.
  • Central nervous system inflammation in EAE impacts glutamatergic synapses.

Purpose of the Study:

  • To investigate the effects of intracerebroventricular (Icv) cladribine administration on EAE.
  • To determine if cladribine offers neuroprotection in experimental MS.
  • To elucidate the mechanism of cladribine's action on synaptic alterations in EAE.

Main Methods:

  • Intracerebroventricular (Icv) infusion of cladribine in EAE mice.
  • Assessment of clinical EAE scores.
  • Electrophysiological recordings to measure excitatory postsynaptic current (sEPSC) frequency.
  • Evaluation of microglial and astroglial activation.
  • Analysis of interleukin-1β (IL-1β) involvement.

Main Results:

  • Icv cladribine administration significantly reduced clinical deficits in EAE mice.
  • Cladribine reversed the EAE-induced enhancement of sEPSC frequency, indicating protection against glutamatergic synaptopathy.
  • Cladribine did not affect EAE-induced microglial or astroglial activation.
  • Cladribine blocked EAE synaptic alterations by interfering with interleukin-1β effects.

Conclusions:

  • Intracerebroventricular cladribine exhibits neuroprotective properties in experimental MS (EAE).
  • Cladribine's neuroprotection in EAE is mediated by interfering with IL-1β effects on synaptic function.
  • These neuroprotective effects are independent of cladribine's peripheral immunosuppressant actions.