Cations Control Lipid Bilayer Memcapacitance Associated with Long-Term Potentiation

Phospholipid bilayers can be described as capacitors whose capacitance per unit area (specific capacitance, C-m) is determined by their thickness and dielectric constant -independent of applied voltage. It is also widely assumed that the C-m of membranes can be treated as a biological constant. Recently, using droplet interface bilayers (DIBs), it was shown that zwitterionic phosphatidylcholine (PC) lipid bilayers can act as voltage-dependent, nonlinear memory capacitors, or memcapacitors. When exposed to an electrical training stimulation protocol, capacitive energy storage in lipid membranes was enhanced in the form of long-term potentiation (LTP), which enables biological learning and long-term memory. LTP was the result of membrane restructuring and the progressive asymmetric distribution of ions across the lipid bilayer during training, which is analogous, for example, to exponential capacitive energy harvesting from self-powered nanogenerators. Here, we describe how LTP could be produced from a membrane that is continuously pumped into a non equilibrium steady state, altering its dielectric properties. During this time, the membrane undergoes static and dynamic changes that are fed back to the system's potential energy, ultimately resulting in a membrane whose modified molecular structure supports longterm memory storage and LTP. We also show that LTP is very sensitive to different salts (KCl, NaCl, LiCl, and TmCl3), with LiCl and TmCl3 having the most profound effect in depressing LTP, relative to KCl. This effect is related to how the different cations interact with the bilayer zwitterionic PC lipid headgroups primarily through electric-field-induced changes to the statistically averaged orientations of water dipoles at the bilayer headgroup interface.

Automated summary

Phospholipid bilayers can act as voltage-dependent memory capacitors, storing energy in the form of long-term potentiation (LTP) during training. LTP is caused by membrane restructuring and asymmetric ion distribution. Different salts have varying effects on LTP.