The intermediate state conformation of the human KCNQ1 potassium channel voltage sensor domain was determined, validated, and shown to be conductive under physiological conditions.
Experimental and computational models reveal how parallel 'core' mechanisms shape direction selectivity at the dendrites of starburst amacrine cells and ganglion cells in the mouse retina.
Computational modeling motivated by recent experiments clarifies biophysical mechanisms generating the rhythm and amplitude of breathing at the level of neurons and brain circuits in mammals.
Optogenetic tools enable sophisticated measurements of a voltage-gated sodium channel implicated in pain, as well as high-throughput screening of candidate channel blockers.
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.
An inducedpluripotent stem cell (iPSC)-based model of KCNQ2-associated developmental epileptic encephalopathy suggests that disease is driven by dyshomeostaic neuronal mechanisms that are downstream of loss of M-current.
The sodium leak NALCN channel functions as a core effector of GABA-B and D2 receptors that is used along with GIRK channels to regulate action potential firing in dopamine neurons.
