I work on health hazards related to water hardness essentially those related to high concentration of calcium with low magnesium concentration. According to the literature, experimental work suggests possible magnesium’s interference with some receptors particularly sensitive receptor N-methyl-D-aspartate. This receptor is active by some amino acids such as aspartate and glutamate which causing stimulation brain function such as learning and memory. Literature has reported that variation in extracellular ionic magnesium concentration from 0.1 to 0.4 mmol significantly reduce the response of central NMDA receptors (Berthelot, 2004).
http://books.google.ht/books?id=VriWntLsQkcC&pg=PA35&lpg=PA35&dq=physiologie+et+regulation+du+magnesium&source=bl&ots=lsmAO1Ngoy&sig=qgW-7obCK6TvPOVsZIW7g_tMcT4&hl=fr&sa=X&ei=2-t6UfvtPJHk8gT884CYBg&ved=0CF0Q6AEwCTgK#v=onepage&q=physiologie%20et%20regulation%20du%20magnesium&f=false
Hi Yanick. The magnesium ion is by definition an antagonist of the NMDA channel. The dissociation constant of magnesium is an exponential function of membrane voltage. If neuronal depolarization, negative electrostatic forces that attracted Mg2 + at the NR2 subunit and collapse the cation is released. This ejection of calcium cap allows, under the action of coagonistes a particularly important calcium influx, so that the depolarization is marked.
Several reports describe how the ability of Mg2+ to block NMDA mediated responses changes as the brain develops, and further suggest that these changes may be regionally dependent. The Mg2+ site is within the cation channel and is occupied at normal membrane potentials which inactivates the NMDA receptor. Depolarisation of neurons, which may be achieved by activation of other glutamate receptors such as the AMPA receptor, is sufficient to overcome the Mg2+ block and allow ion flow through the cation channel.
The normal voltage dependent block of channels by Mg2+ is highly important for the sort of functions NMDA receptors have to perform. The block is only relieved by an appropriately timed depolarisation of the neuron which may be brought about by activation of other types of glutamate receptor, including the fast acting AMPA subtype. Membrane depolarisation to remove the block of channels by Mg2+ is a prerequisite for NMDA activation and synaptic plasticity, whereas protracted or intense NMDA activation may cause neural injury such as follows cerebral ischaemia. The age related alteration in Mg2+ efficacy reported here may reflect a fine tuning of NMDA receptors so that the relative ease or difficulty in
removing the Mg2+ block with depolarisation varies as the trophic and other functions of NMDA receptors are adjusted in the developing brain.
I am pleased to send you a document which explain the " Modulation by magnesium of N-methyl-D-aspartate receptors in developing human brain."
I thank you again Islande because you share this document with me. It’s very interesting. In relation to the potential clinical uses of magnesium sulphate in man, the literature has shown how NMDA receptors in neonatal brain are affected by Mg2+. The Mg2+ IC value was higher in neonatal brain (3.6 mM) than infant (1.4 mM) and adult (0.87mM) brains. How can you explain the variation of Mg2+ IC for neonatal brain, infant and adult?
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