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Q J Med 1999; 92: 133-141
© 1999 Association of Physicians

Mini-review

Calcium channelopathies

M.G. Benatar

From the Department of Medicine (Neurology), Groote Schuur Hospital, Cape Town, South Africa

Dr M.G. Benatar, Beth Israel Deaconess Medical Center—East, 330 Brookline Avenue, Medicine, GZ-207, Boston, Massachusetts 02115, USA. e-mail: mbenatar@caregroup.harvard.edu

Introduction

Calcium (Ca2+) is an essential signalling molecule in many biological systems, and normal intracellular calcium levels at ~100 nM are 20 000-fold lower than the 2 mM concentration found extracellularly. Homoeostatic mechanisms are tightly controlled to enable Ca2+ to mediate a variety of cellular functions and to prevent sustained rises in intracellular calcium concentration which result in cell death.

Abnormalities of calcium homoeostasis are recognized to play an important role in the excitotoxic damage which occurs in the setting of cerebrovascular disease and various neurodegenerative diseases.1 More recently, however, abnormalities of the voltage-gated calcium channel (VGCC), one of the key regulators of intracellular calcium concentration, have been implicated in a wide range of human diseases, including migraine,2 episodic ataxia,2 spinocerebellar degeneration,3 the Lambert-Eaton myasthenic syndrome,4 hypokalaemic periodic paralysis5 and X-linked congenital stationary night blindness (xlCSNB).6,7 It has been suggested that amyotrophic lateral sclerosis may be mediated by antibodies . . . [Full Text of this Article]

VGCC structure and function

The Lambert-Eaton myasthenic syndrome (LEMS)

The muscular dysgenesis mouse, hypokalaemic periodic paralysis and malignant hyperthermia

Familial hemiplegic migraine, episodic ataxia-2 and spinocerebellar ataxia-6

X-linked congenital stationary night blindness

Amyotrophic lateral sclerosis

The Tottering, Leaner, Lethargic andStargazer mice

Discussion

Conclusion

Acknowledgements

References


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M. Benatar
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QJM, December 1, 2000; 93(12): 787 - 797.
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