Magnesium calms nerves

Magnesium has a calming effect on the nervous system

The neurological effects of magnesium

Mg++ (at high extracellular concentration) reduces electrical excitation by diminishing synaptic transmission.  Achieved via blocking release of acetylcholine into the synaptic gap between neurons.

Mg++ reduces neuronal excitability in its role as a natural “Calcium Channel Blocker”.     Mg++ ions (and other ++ cations at mM concentrations) decrease the activation of certain membrane-bound, voltage-gated calcium channels, and in limiting the influx of extracellular calcium++ into the neuronal cytosol, thereby reduce neuronal excitability.

Mg++ reduces pain.   By blocking N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system; prevents ion-flow at typical neuronal resting potentials.  Mayer, 1987

Mg is a “calcium channel blocker” in neurons

Mg++ at high extracellular concentrations blocks Ca++influx and diminishes synaptic transmission.  Dodge, 1967

If Mg levels are low, nerves lose control over muscle activity, respiration and mental processes.   Nerve cells (neurons) need sufficient magnesium to give or receive messages, without which they become excitable and highly reactive. This causes the person to become highly sensitive and highly nervous, possibly resulting in:

# E.g. sharp muscle reaction to an unexpected loud noise.

These effects manifest themselves in several well-known neurological /neuromuscular conditions.    Including sleep disorders, the “shakes”in alcoholics, Parkinson's disease, migraines, pre-eclampsia, suicidal tendencies, epileptic seizures, pain, SIDS, CFS and psychiatric disorders:

Magnesium for Neurological/ Neuromuscular conditions

Mg is cofactor for ATPase pumps / ATP production

ATP-producing mitochondria are highly concentrated in cells of the brain and central nervous system.    Since neurotransmission has an avid need for ATP energy

Mg for Cell "Battery"/ATP Production

References

Dodge Jr FA, Rahamimoff R. Co-operative action a calcium ions in transmitter release at the neuromuscular junction. J Physiol 1967; 193: 419-432.   PubMed

Mayer ML, Westbrook GL. Permeation and block of N-methyl-D-aspartic acid receptor channels by divalent cations in mouse cultured central neurones. J Physiol 1987; 394: 501-527.PubMed