Neuronal neurofascin takes a surprisingly circuitous route in the neuronal plasma membrane to the axon initial segment where it stabilises ion channel complexes responsible for initiating action potentials.
A potassium channel, as a nonconducting function, organizes compartmentalized neuronal calcium signaling microdomains via structural and functional coupling of plasma membrane and endoplasmic reticulum calcium channels.
Short, theta-bursts of action potential firing decrease the global excitability of CA1 pyramidal neurons, providing an internal mechanism which could regulate their allocation to memory engrams.
The pairing of chemogenetic and electrophysiological approaches reveals mechanisms by which cholinergic synapses modulate the final motor output of the nervous system.
The tarantula toxins psalmotoxin and guangxitoxin have a similar concave surface for interacting with α-helices in voltage-gated and acid-sensing ion channels.
Electrophysiology measurements characterized eight optogenetic methods, including a new reporter mouse expressing soma-localized light-activated chloride channels, for inactivating small regions of mouse neocortex.
Polyunsaturated fatty acid analogues show selectivity for different cardiac ion channels, suggesting their potential use for the treatment of different subtypes of Long QT Syndrome.
The structure of a voltage-activated potassium channel in lipid nanodiscs solved using cryo-electron microscopy is similar to previous X-ray structures, and provides insights into the mechanism of C-type inactivation.
Contrary to a generally accepted principle, the pore properties of KCNQ1 channels depend on the states of voltage-sensing domains activation; KCNE1 alters the voltage-sensing domains-pore coupling to modulate KCNQ1 channel properties.
