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.