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Iseri, L.T. and French, J.H. (1984) Magnesium: Nature’s physiologic calcium blocker. American Heart Journal, 108, 188-193. doi:10.1016/0002-8703(84)90572-6

has been cited by the following article:

  • TITLE: Pharmacological evaluation of catalepsy in low calcium and/or magnesium deficient feeding mice

    AUTHORS: Osamu Nakagawasai, Ryoo Taniguchi, Koichi Tan-No, Fumihiro Yamadera, Wataru Nemoto, Fukie Yaoita, Takeshi Tadano

    KEYWORDS: Calcium; Catalepsy; Dopamine; Magnesium

    JOURNAL NAME: Health, Vol.4 No.11A, November 29, 2012

    ABSTRACT: Populations from the Kii peninsula of Japan and Guam present a high incidence of amyotrophic lateral sclerosis and parkinsonism-dementia complex. It is thought that the low levels of calcium (Ca) and magnesium (Mg) in the drinking water are involved in the pathogenesis of these diseases. The present study aimed to test the hypothesis that catalepsy, a behavioral immobility and one of the Parkinsonian symptoms, may result from functionally impaired dopaminergic neurons in low Ca and Mg (LCa/Mg) fed mice. A group of mice fed with an LCa/Mg diet for 6 weeks was compared to a control group on a standard diet. Cataleptic symptoms such as akinesia and rigidity were measured using the bar test. The antiparkinsonian drugs dopamine (DA) precursor L-3, 4-dihydroxy phenylamine (L-DOPA), the selective DA receptor D2 agonist bromocriptine and the DA releaser amantadine were tested for their effects on the induced catalepsy. Mice developped catalepsy after 3 weeks on the LCa/Mg diet. LCa/Mg diet-induced catalepsy was improved by the administration of either L-DOPA (50 - 200 mg/kg i.p.) in combination with benserazide (25 mg/kg i.p.), bromo- criptine (0.25 - 4 mg/kg i.p.) or amantadine (5 - 20 mg/kg i.p.). These results suggest that catalepsy in LCa/Mg mice might result from a hypofunction of dopaminergic neurons. Moreover, our results support the hypothesis that LCa/Mg in-take may be one etiological factor in neurodegenerative disorders including Parkinson’s disease.