Chloride channels and cation-chloride cotransporters play in concert to control neuronal excitability. Loss of function of potassium-chloride KCC3 in humans and mice induces severe sensory-motor neuropathy and decreased KCC2 is responsible for spasticity following spinal cord trauma. Expression of calcium-activated chloride channels in spinal motoneurons could play a role in the control of motoneuron excitability under pathophysiological conditions. Our research goal is to uncover cellular mechanisms linking chloride homeostasis to motoneuron excitability in a neuroinflammatory context.

image 5 2 1


Chloride channels (red) are expressed in motoneurons (blue) at the level of synaptic inputs

Motoneuron 3.2


Motoneuron electrical activity.

image 5 2 3


In vitro model of a functional neuromuscular junction to decipher cell-type contributions to early neuromuscular dysfunction in ALS, SMA and Anderman syndrome.

 (green, Hb9::GFP motoneuron-phase contrast, SOD1G93A myotube with recording electrode)





Major publications

Bowerman M., et al., Neurobiol Dis. 2017

Bowerman M., et al., Hum Mol Genet. 2015

Rousset M., et al., Neuropharmacology. 2015

Benzina O., et al., PLoS One. 2014

Pieraut S., et al., J Neurosci. 2011



  • Csilla Gergely, Charles Coulomb laboratory, Montpellier
  • Melissa Bowerman, Keele University, UK
  • Pierre Charnet, IBMM, Montpellier
  • Pierre-François Méry, IGF, Montpellier



Scamps Frédérique