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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.

NALCN and TRPC6 drive the subthreshold depolarization of VTA DA neurons and down regulation of TRPC6 contributes to reduced VTA DA neuron firing and chronic stress-induced depression-like behavior of mice.

Tricyclic antidepressants activate lysosomal two-pore Na⁺ channels in a voltage-dependent manner.

Electrophysiological and computational techniques provide a structural basis for understanding the conformational changes that are required to activate Hv1 proton channels.

The positioning of AMPA-type glutamate receptors at synapses – a requirement for effective neurotransmission and synaptic plasticity – is orchestrated by their extracellular, N-terminal domain.

Allosteric gating in a transient receptor potential channel is modulated by external sodium ions and a tarantula toxin.

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.

TMEM16F shifts its ion selectivity in response to change of intracellular Ca²⁺, membrane potential and ionic strength.

TMEM206 proteins are identified as constituting the pore of the widely expressed acid-activated chloride channel PAORAC/ASOR, which is important in acid toxicity.

Neurons in the hypothalamus that promote satiety manifest plasticity of their response to the excitatory transmitter, glutamate, by re-organizing the composition of a specific glutamare receptor.