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.
A ClC chloride channel protein allows neurons to interpret both temporal resolution and intensity of sensory input, which thereby contributes to an experience-dependent navigation behavior.
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.
ADGRG2, an orphan GPCR, when coupled to CFTR via a regional Gq signaling on the apical membrane, acts to regulate efferent duct fluid reabsorption making it essential for male fertility.
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.
Prenatal ethanol exposure results in aberrant tangential migration by altering NKCC1-mediated chloride homeostasis that can be mitigated by bumetanide.