In excitable cells, the concentration of intracellular free Mg²⁺ ([Mg²⁺]_i) is several hundred times lower than expected if Mg²⁺ ions were at electrochemical equilibrium. Since Mg²⁺ is a permeant ion across the plasmalemma, it must be constantly extruded. An ATP-dependent Na/Mg exchanger has been proposed as the sole mechanism responsible for Mg²⁺ extrusion. However, this hypothesis fails to explain numerous observations including the fact that K⁺ and Cl^- appear to be involved in Mg²⁺ transport. Until now three main limitations have hampered the studies of plasmalemmal Mg²⁺ transport: i) ²⁸Mg, the only useful radioactive isotope of Mg²⁺, has a short half-life and is difficult to obtain; ii) squid giant axons, the ideal preparation to carry out transport studies under "zero-trans" conditions, are only available during the summer months; and iii) the ionic fluxes mediated by the Mg²⁺ transporter are very small and difficult to measure. The purpose of this manuscript is to review how these limitations have been recently overcame and to propose a novel hypothesis for the plasmalemmal Mg²⁺ transporter in squid axons and barnacle muscle cells. Overcoming the limitations for studying the plasmalemmal Mg²⁺ transporter has been possible as a result of the following findings: i) the Mg²⁺ exchanger can operate in "reverse", thus extracellular Mg²⁺-dependent ionic fluxes (e.g., Na⁺ efflux) can be utilized to measure its activity; ii) internally perfused, voltage-clamped barnacle muscle cells which are available all year long can be used in addition to squid axons; and iii) phosphoinositides (e.g., PIP₂) produce an 8-fold increase in the ionic fluxes mediated by the Mg²⁺ exchanger. The hypothesis that we postulate is that, in squid giant axons and barnacle muscle cells, a 2Na+2K+2Cl:1Mg exchanger is responsible for transporting Mg²⁺ across the plasmalemma and for maintaining [Mg²⁺]_i under steady-state conditions.