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.
Chloride channels (red) are expressed in motoneurons (blue) at the level of synaptic inputs
Motoneuron electrical activity.
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)
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- Csilla Gergely, Charles Coulomb laboratory, Montpellier
- Melissa Bowerman, Keele University, UK
- Pierre Charnet, IBMM, Montpellier
- Pierre-François Méry, IGF, Montpellier