Spinal Motoneuron TMEM16F Acts at C-boutons to Modulate Motor Resistance and Contributes to ALS Pathogenesis

Abstract

Soulard et al. show that TMEM16F, a calcium-activated chloride channel, is a post-synaptic component of C-boutons that contributes to the excitability of fast α-motoneurons. They find that the loss of TMEM16F function leads to reduced performance during motor-demanding tasks but improves motor functions of male mice with amyotrophic lateral sclerosis.