Mathematical models with experimental validation show that chloride transporters in the cell membrane, and not negatively charged impermeant molecules, generate the driving force used by GABA receptors to silence neurons.
Electrophysiological and simulation approaches show that a chloride-related longer relaxation of the inhibitory synaptic events partially compensates the early defect in the chloride homeostasis detected in fetal SOD spinal motoneurons.
Modifying membrane potential by an 'inhibitory' chloride conductance such as PSAM4-GlyR is inherently unstable because the normally low intracellular concentration of chloride is readily increased by influx of chloride.
The chloride channel Ano1/Tmem16a plays an essential and non-redundant role in the developing airway by inhibiting mucus cell hyperplasia and promoting proper immune function of the airway mucosal barrier.
The effects of chloride homeostasis can explain diverse responses of basal ganglia output neurons to putatively inhibitory inputs and may tune these neurons' synchrony, oscillations and behavior in decision-making scenarios.