Maintaining a membrane electrical potential of biological cells is a dynamic process, as some cells have a continually changing potential, like pacemaker cells, while other cells may function with large or small changes in the membrane potential. Additionally, some cells may change their electrical potential when stimulated or inhibited by electrical signals, chemical compounds, or both—either simultaneously or episodically. The persistent leak of K+ through two-pore-domain potassium channels (K2P) and of Na+ through Na+ leak channels (NALCNs) and the action of pumps and exchangers are primarily responsible for maintaining a resting potential. Ca2+ ions are known to block the NALCNs and result in a more hyperpolarized membrane potential, with a reduction in Ca2+ resulting in a depolarized state. Using the larval muscles of Drosophila, the membrane potentials were monitored as Ca2+ and Mg2+ concentrations were altered. Changes as large as 20 mM of Mg2+ had only small effects (1 to 2 mV) on the membrane potential compared to 3–5 mM changes in Ca2+ having larger effects (5–10 mV). Although, it appears raised Mg2+ may dampen the changes induced by Ca2+. Simulations of the G-H-K equation estimate the changes in permeability of Na+ (pNa). These experiments are significant, as the clinical severity of hypocalcemia and hypercalcemia may also depend on Mg2+ levels.
Hana et al. (Mon,) studied this question.