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Related Experiment Video

Updated: Apr 27, 2026

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Chronic p75 neurotrophin receptor modulation with LM11A-31 attenuates seizure progression and network

Esra Kabak1, Selcen Aydin-Abidin2, Ayşe Yeşim Göçmen3

  • 1Department of Biophysics, Graduate School of Health Sciences, Karadeniz Technical University, Trabzon, Türkiye.

Neuropharmacology
|April 25, 2026
PubMed
Summary

LM11A-31, a p75 neurotrophin receptor (p75NTR) modulator, effectively reduced seizure severity and network hyperexcitability in a pentylenetetrazole (PTZ) kindling model. This treatment also mitigated synaptic, inflammatory, and oxidative damage, suggesting therapeutic potential for epilepsy.

Keywords:
Electrocorticography (ECoG)LM11A-31NeuroinflammationPTZ kindlingSynaptic proteinsp75 neurotrophin receptor

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • The pro-nerve growth factor (proBDNF)/p75 neurotrophin receptor (p75NTR) pathway is implicated in neuronal hyperexcitability and epileptogenesis.
  • Understanding the role of p75NTR signaling in seizure progression is crucial for developing novel epilepsy treatments.

Purpose of the Study:

  • To investigate the efficacy of the small-molecule ligand LM11A-31 in modulating p75NTR signaling.
  • To determine if LM11A-31 attenuates seizure progression and network dysfunction in a pentylenetetrazole (PTZ)-induced kindling model.

Main Methods:

  • Male C57BL/6 mice were subjected to PTZ kindling, with LM11A-31 administered pre-emptively and throughout the experiment.
  • Seizure severity was assessed using Racine scoring and cumulative seizure burden.
  • Electrocorticography (ECoG) was used to measure network hyperexcitability (power and RMS amplitude).
  • Synaptic proteins, inflammatory markers, and oxidative stress indices were quantified in cortical and hippocampal tissues.

Main Results:

  • LM11A-31 significantly reduced PTZ-induced seizure severity and cumulative seizure burden.
  • The drug normalized increased cortical ECoG power and RMS amplitude, indicating reduced network hyperexcitability.
  • LM11A-31 treatment restored levels of synaptic proteins (PSD-95, synaptophysin) and reduced elevated TNF-α levels.
  • Antioxidant capacity was partially restored, while oxidant load and lipid peroxidation were decreased.

Conclusions:

  • Pharmacological modulation of p75NTR signaling with LM11A-31 effectively suppresses seizure progression in a PTZ kindling model.
  • LM11A-31 mitigates key pathological alterations, including electrophysiological, synaptic, inflammatory, and oxidative changes associated with kindling.
  • These findings highlight the therapeutic potential of targeting the p75NTR pathway for epilepsy treatment.