Chung considers a new model that describes how a muscle responds to stretch and its implications on myosin detachment and physiology.
Palmer et al. demonstrate that a stretch-induced enhancement of the myosin crossbridge detachment rate is sufficient to explain the force response of cardiac muscle to a quick stretch and would benefit diastolic function in a beating heart.
The mechanisms shaping CA2 pyramidal neuron action potential bursting induced by muscarinic acetylcholine receptor activation
Robert et al. reveal that muscarinic receptor activation causes hippocampal CA2 pyramidal neurons to depolarize and fire bursts of action potentials. The properties of these bursts are regulated by synaptic inputs, as well as T-type calcium channels, D-type potassium channels, and SK channels.
Mutations in the pre-M1 helix of NMDA receptor subunits are associated with neurological disease. McDaniel et al. reveal that the helix influences channel gating, potentially through interactions with a network of aromatic amino acids within the subunit’s pre-M1 and pore-forming M3 helices and the adjacent subunit’s M4 helix.
Structure of KCNH2 cyclic nucleotide-binding homology domain reveals a functionally vital salt-bridge
Human KCNH2 are key channels governing cardiac repolarization. Here, a 1.5 Å resolution structure of their cyclic nucleotide-binding homology domain is presented. Structural analysis and electrophysiological validation reveal a novel salt-bridge that plays an important role in hKCNH2 functional regulation.