Features of Central Neurotransmission in Animals in Conditions of Dietary Magnesium Deficiency and After Its Correction

Abstract

Magnesium is important in the regulation of neurotransmitter metabolism and the modulation of receptor function in the CNS, including neurotransmitters and receptors involved in the pathogenesis of many mental disorders. The aim of the present work was to perform a pharmacological evaluation of the central mechanisms of action of magnesium salts in the clofelin, phenamine, arecoline, nicotine, apomorphine, and 5-hydroxytryptophan tests in conditions of dietary magnesium deficiency. After reaching the magnesium deficiency state, animals were given oral (via tube) magnesium L-asparaginate and magnesium chloride lone and in combination with vitamin B(6), as well as the reference agent Magne B6. Our assessments of phenamine stereotypy in magnesium-deficient animals showed reductions in the latent period by an average of 14.89% and a significant increase in the duration of phenamine stereotypy by an average of 19.44% (from 268.23 +/- 8.17 to 320.36 +/- 19.90 min) as compared with intact rats. Studies of hyperkinesia induced by 5-hydroxytryptophan showed a two-fold reduction in its extent in the magnesium-deficient group (p </= 0.05). Administration of arecoline to magnesium-deficient animals resulted in a statistically significant increase in the latent period from a mean of 92.75 +/- 19.35 to 245.17 +/- 121.86 sec, with a reduction in the duration of tremor from an average of 1175.58 +/- 127.87 to 703.83 +/- 89.33 sec (p </= 0.05) as compared with intact rats. In terms of its influence on the hypothermic effects of clofelin and apomorphine and the convulsive effect of nicotine, there were no significant differences between the intact group and the magnesium-deficiency animals. Administration of magnesium salts compensated for the magnesium deficiency in plasma and erythrocytes, which was accompanied by recovery of measures in the phenamine, arecoline, and 5-HT tests to levels typical of intact controls. There was a tendency for magnesium L-asparaginate and magnesium chloride combined with pyridoxine to have greater activity, and the efficacies of these treatments was no less than that of reference agent Magne B6. Thus, dietary magnesium deficiency led to impairment of neurotransmission in central serotoninergic, M-cholinergic, and noradrenergic structures and administration of magnesium salts reversed these changes.

The Role and the Effect of Magnesium in Mental Disorders: A Systematic Review

“…Magnesium is essential to ensure the correct functioning of all human cells, neurons included; it is involved, among others processes, in hundreds of enzymatic reactions [ 28 ], intracellular transmission [ 29 ], myelination process [ 30 ], synapses formation and maintenance [ 31 ] as well as in the regulation of serotoninergic, dopaminergic and cholinergic transmission [ 32 ]. Magnesium is, therefore, an element necessary to maintain neurons healthy and viable [ 33 ], especially because it has been shown to reduce apoptosis in an animal model of induced hypoxia-ischemia [ 34 ] and to prevent synaptic loss in a mouse model of Alzheimer disease [ 35 , 36 ].…”

Can Nutrients and Dietary Supplements Potentially Improve Cognitive Performance Also in Esports?

“…It plays a role in protecting against overstimulation that leads to cellular death: It interacts with the aspartate receptor to block the calcium channel at that receptor and must be cleared for glutamatergic excitatory signaling to occur. Low levels of magnesium may theoretically increase glutamatergic neurotransmission, which may lead to oxidative stress and nerve cell death [ 82 ]. The vast majority of studies conducted so far have focused on depression, due to the recognized role of magnesium in several basic mechanisms of the pathophysiology of depression, including inflammation and oxidative stress [ 61 ] ( Table 1 ).…”

“…The results of the present research indicate that magnesium deficiency may contribute to weakening of the body, manifested, e.g., by dizziness, fatigue, lethargy, lightheadedness, and loss of appetite [ 83 , 84 ]. Additionally, magnesium deficiency may lead to the formation of oxidative stress, thereby increasing the risk of depression, as well as problems with concentration, working memory, and attention, which are required for gaming [ 61 , 82 ]. Therefore, it is worth ensuring an adequate supply of magnesium in the diets of e-athletes to prevent the negative effects of a deficiency of this element.…”

Basic considerations on magnesium in the management of neurocritical patients

“…Mg facilitates organic activities in the neuromuscular system, such as neuronal and muscular excitability, contractibility, and rhythm in the cardiovascular system, and vasodilatation in the circulatory system [25][26][27]. More specifically, in the brain, it is responsible for intracellular transmission, myelination, synapse formation and maintenance, and regulation of cholinergic, dopaminergic, and serotonergic transmission (through the decrease of acetylcholine release at the neuromuscular junction; blockade of N-methyl-D-aspartate (NMDA) receptors, inhibiting the excitatory function of glutamate, and stimulation of GABA receptors generating neuronal hyperpolarization, and exerting an inhibitory effect in the process) [28][29][30][31]. It is also involved in the release of calcitonin gene-related peptide (neuropeptide).…”