Abstract
Magnesium ions have many cellular actions including the suppression of the excitability of neurons; however, the depolarization effect of magnesium ions seems to be contradictory. Thus several hypotheses have aimed to explain this effect. In this study, a quantum mechanical approach is used to explain the depolarization action of magnesium. The model of quantum tunneling of magnesium ions through the closed sodium voltage-gated channels was adopted to calculate the quantum conductance of magnesium ions, and a modified version of Goldman–Hodgkin–Katz equation was used to determine whether this quantum conductance was significant in affecting the resting membrane potential of neurons. Accordingly, it was found that extracellular magnesium ions can exhibit a depolarization effect on membrane potential, and the degree of this depolarization depends on the tunneling probability, the channels’ selectivity to magnesium ions, the channels’ density in the neuronal membrane, and the extracellular magnesium concentration. In addition, extracellular magnesium ions achieve a quantum conductance much higher than intracellular ones because they have a higher kinetic energy. This study aims to identify the mechanism of the depolarization action of magnesium because this may help in offering better therapeutic solutions for fetal neuroprotection and in stabilizing the mood of bipolar patients.
Highlights
Magnesium has several uses in the medical field
One contradictory feature of magnesium has been documented. This feature is the ability of magnesium ions to depolarize resting membrane potential, which increases the excitability of neurons in contrast to the actual actions of magnesium, but the overall net effect is to suppress excitability [2,3]
The forbidden region for extracellular magnesium ions is from X1 = 2.64 × 10−11 m to X2 = 5.4 × 10−11 m, and the forbidden region for intracellular magnesium ions is from X1 = 0.18 × 10−11 m to X2 = 5.4 × 10−11 m
Summary
Magnesium has several uses in the medical field. It is used to treat eclampsia, asthmatic patients, and certain cardiac arrhythmias. Magnesium is a crucial cofactor for enzymes, and it is vital for ATP production [1]. Magnesium depolarizes the action potential threshold, decreases the frequency of action potentials, and suppresses the overall activity and excitability of neurons. One contradictory feature of magnesium has been documented. This feature is the ability of magnesium ions to depolarize resting membrane potential, which increases the excitability of neurons in contrast to the actual actions of magnesium, but the overall net effect is to suppress excitability [2,3]
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