Whole endosome recording shows that chloride interacts with vesicular glutamate transporters as both allosteric activator and permeant ion, and although the mode of permeation differs, chloride and glutamate use a related conduction pathway.
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.
A computer model of human cardiomyocyte was produced and validated on independent datasets, overcoming shortcomings of its predecessors, also yielding broadly relevant insights and results on major ionic currents.
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.
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.
Combined simulations and electrophysiological experiments show that the CLC channels and exchangers form physically distinct and evolutionarily conserved pathways through which Cl- and H+ ions move when crossing biological membranes.
Cytotoxicity associated with APOL1 renal-risk variants occurs through its plasma-membrane localization, where aberrant channel activity drives a sustained sodium and calcium influx leading to cell swelling and eventually cell death.
Novel evidence on the molecular determinants of the dual function, anion permeation and substrate transport, of excitatory amino acid transporters opens avenues toward illuminating how these transporters regulate synaptic function and contribute to neurological conditions.