Lateral diffusion of ions near membrane surface.

Biological membranes isolate living cells from their environment, while allowing selective molecular transport between the inner and outer realms. For example, Na and K permeability through ionic channels contributes to neural conduction. Whether the ionic currents arise directly from cations in the bulk, or from the interface, is currently unclear. There are only scant results concerning lateral diffusion of ions on aquated membrane surfaces (and strong belief that this occurs through binding to a diffusing lipid). We performed classical molecular dynamics (MD) simulations of monovalent ions, Na, K, and Cl, near the surface of the zwitterionic palmitoyl-oleoyl-phosphatidylcholine (POPC) membrane. Realistic force-fields for lipids (Amber's Lipid17 and Lipid21) and water (TIP4P-Ew) are tested for the mass and charge densities and the electrostatic potential across the membrane. These calculations reveal that the chloride can bind to the choline moiety through an intervening water molecule by forming a CH⋯OH hydrogen bond, while cations bind to both the phosphatic and carbonyl oxygens of phosphatidylcholine moieties. Upon transitioning from the bulk to the interface, a cation sheds some of its hydration water, which are replaced by headgroup atoms. Notably, an interfacial cation can bind 1-4 headgroup atoms, which is a key to understanding its surface hopping mechanism. We find that cation binding to three headgroup atoms immobilizes it, while binding to four energizes it. Consequently, the lateral cation diffusion rate is only 15-25 times slower than in the bulk, and 4-5 times faster than lipid self-diffusion. K diffusion is notably more anomalous than Na, switching from sub- to super-diffusion after about 2 ns.