Neurotrophic Properties of C-Terminal Domain of the Heavy Chain of Tetanus Toxin on Motor Neuron Disease.

Mireia Herrando Grabulosa*, Catalina Casas Louzao, Kevin Talbot, Jose Aguilera

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

Abstract

The carboxyl-terminal domain of the heavy chain of tetanus toxin (Hc-TeTx) exerts a neuroprotective effect in neurodegenerative diseases via the activation of signaling pathways related to neurotrophins, and also through inhibiting apoptotic cell death. Here, we demonstrate that Hc-TeTx preserves motoneurons from chronic excitotoxicity in an in vitro model of amyotrophic lateral sclerosis. Furthermore, we found that PI3-K/Akt pathway, but not p21ras/MAPK pathway, is involved in their beneficial effects under chronic excitotoxicity. Moreover, we corroborate the capacity of the Hc-TeTx to be transported retrogradely into the spinal motor neurons and also its capacity to bind to the motoneuron-like cell line NSC-34. These findings suggest a possible therapeutic tool to improve motoneuron preservation in neurodegenerative diseases such as amyotrophic lateral sclerosis.

Original languageEnglish
Article number12
Pages (from-to)666-675
Number of pages11
JournalToxins
Volume12
Issue number10
DOIs
Publication statusPublished - 21 Oct 2020

Keywords

  • Amyotrophic lateral sclerosis
  • Carboxyl-terminal domain of the heavy chain of tetanus toxin
  • Excitotoxicity
  • Neuroprotection
  • Spinal muscular atrophy

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