A computer model predicts different mechanisms of blood pressure regulation and effective hypertensive therapy for males and females, thereby serving as a foundational tool for improved treatment precision.

Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.

At distal synapses onto hippocampal CA1 pyramidal neurons, synaptic plasticity is dependent on dendritically initiated sodium spikes, thus establishing a new role for voltage-gated sodium channels in the dendrites that may have important implications for how learning rules are implemented.

FRET biosensor-based measurement of cAMP signaling and single-channel recording reveal that β-blockers trigger local activation of adrenergic receptors and calcium channels in primary neurons.

High-speed calcium imaging from the axon initial segment shows that sodium channels are in part permeable to calcium ions.

A cationic molecule derived from an uncharged Cav2.2 calcium channel inhibitor powerfully inhibits both sodium and calcium channels with extracellular application and inhibits both pain and neurogenic inflammation.

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.

Outward calcium ion currents desensitize the human PKD2-L1 ion channel via a mechanism that is independent of cytosolic motifs.

The centipede peptide toxin SpTx1 blocks the pore of ATP-sensitive potassium channels in pancreatic β cells to markedly enhance insulin secretion and mitigate hyperglycemia in diabetic mice insensitive to the anti-diabetic sulfonylurea glibenclamide.

A multi-scale integration of experimental and computational approaches shows how a non-linear dependence of T-type calcium channel gating on GABA_B receptor activity regulates thalamic network oscillations.