NeuroMolecular Medicine

, Volume 8, Issue 3, pp 307–318 | Cite as

Calcium channelopathies

  • Ricardo Felix
Review Article


Intracellular calcium ([Ca2+] i ) is highly regulated in eukaryotic cells. The free [Ca2+] i is approximately four orders of magnitude less than that in the extracellular environment. It is, therefore, an electrochemical gradient favoring Ca2+ entry, and transient cellular activation increasing Ca2+ permeability will lead to a transient increase in [Ca2+] i . These transient rises of [Ca2+] i trigger or regulate diverse intracellular events, including metabolic processes, muscle contraction, secretion of hormones and neurotransmitters, cell differentiation, and gene expression. Hence, changes in [Ca2+] i act as a second messenger system coordinating modifications in the external environment with intracellular processes. Notably, information on the molecular genetics of the membrane channels responsible for the influx of Ca2+ ions has led to the discovery that mutations in these proteins are linked to human disease. Ca2+ channel dysfunction is now known to be the basis for several neurological and muscle disorders such as migraine, ataxia, and peri odic paralysis. In contrast to other types of genetic diseases, Ca2+ channelopathies can be studied with precision by electrophysiological methods, and in some cases, the results have been highly rewarding with a biophysical phenotype that correlates with the ultimate clinical phenotype. This review outlines recent advances in genetic, molecular, and pathophysiological aspects of human Ca2+ channelopathies.

Index Entries

Absence epilepsy Ca2+ channels cerebellar ataxia CSNB2 EA2 FHM1 HypoPP MHS SCA6 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Adams B. A., and Beam K G. (1990) Muscular dys genesis in mice: a model system for studying excitation-contraction coupling. FASEB J. 4, 2809–2816.PubMedGoogle Scholar
  2. Arikkath J., and Campbell K. P. (2003) Auxiliary subunits: essential components of the voltage-gated calcium channel complex. Curr. Opin. Neurobiol. 13, 298–307.PubMedCrossRefGoogle Scholar
  3. Bain P. G., O'Brien M. D., Keevil F., and Porter D. A. (1992) Familial periodic cerebellar ataxia: a problem of cerebellar intracellular pH homeostasis. Ann. Neurol. 31, 147–154.PubMedCrossRefGoogle Scholar
  4. Ball S. L., and Gregg R. G. (2002) Using mutant mice to study the role of voltage-gated calcium channels in the retina. Adv. Exp. Med. Biol. 514, 439–450.PubMedGoogle Scholar
  5. Ball S. L., Powers P. A., Shin H. S., Morgans C. W., Peachey N. S., and Gregg R. G. (2002) Role of the β2 subunit of voltage-dependent calcium channels in the retinal outer plexiform layer. Invest. Ophthalmol. Vis. Sci. 43, 1595–1603.PubMedGoogle Scholar
  6. Baloh R. W. and Jen J. C. (2002) Genetics of familial episodic vertigo and ataxia. Ann. NY Acad. Sci. 956, 338–345.PubMedCrossRefGoogle Scholar
  7. Bech-Hansen N. T., Boycott K. M., Gratton K. J., Ross D. A., Field L. L., and Pearce W. G. (1998a) Local ization of a gene for incomplete X-linked congenital stationary night blindness to the interval between DXS6849 and DXS8023 in Xp11.23. Hum. Genet. 103, 124–130.PubMedCrossRefGoogle Scholar
  8. Bech-Hansen N. T., Naylor M. J., Maybaum T. A., et al. (1998b) Loss-of-function mutations in a calcium-channel α1 subunit gene in Xp11.23 cause incomplete X-linked congenital stationary night blindness. Nat. Genet. 19, 264–267.PubMedCrossRefGoogle Scholar
  9. Birnbaumer L., Campbell K. P., Catterall W. A., et al. (1994) The naming of voltage-gated calcium channels. Neuron 13, 505, 506.PubMedCrossRefGoogle Scholar
  10. Black J. L. 3rd. (2003) The voltage-gated calcium channel γ subunits: a review of the literature. J. Bioenerg. Biomembr. 35, 649–660.PubMedCrossRefGoogle Scholar
  11. Boycott K. M., Maybaum T. A., Naylor M. J., et al. (2001) Asummary of 20 CACNA1F mutations identified in 36 families with incomplete X-linked congenital stationary night blindness, and characterization of splice variants. Hum. Genet. 108, 91–97.PubMedCrossRefGoogle Scholar
  12. Brooks C., Robinson R. L., Halsall P. J., and Hopkins P. M. (2002) No evidence of mutations in the CACNA1S gene in the UK malignant hyperthermia population. Br. J. Anaesth. 88, 587–589.PubMedCrossRefGoogle Scholar
  13. Catterall W. A. (2000) Structure and regulation of voltage-gated Ca2+ channels. Annu. Rev. Cell Dev. Biol. 16, 521–555.PubMedCrossRefGoogle Scholar
  14. Catterall W.A., Perez-Reyes E., Snutch T. P., and Striessnig J. (2005) International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels. Pharmacol. Rev. 57, 411–425.PubMedCrossRefGoogle Scholar
  15. Chartrand D. (2003) Rapid intervention for an episode of malignant hyperthermia. Can. J. Anaesth 50, 104–107.PubMedCrossRefGoogle Scholar
  16. Chen X. H., Bezprozvanny I., and Tsien R. W. (1996) Molecular basis of proton block of L-type Ca2+ channels. J. Gen. Physiol. 108, 363–374.PubMedCrossRefGoogle Scholar
  17. Christopher A. R. (1997) Intranuclear neuronal inclusions: a common pathogenic mechanism for glutamine-repeat neurodegenerative diseases? Neuron 19, 1147–1150.CrossRefGoogle Scholar
  18. Davies N. P. and Hanna M. G. (2001) The skeletal muscle channelopathies: basic science, clinical genetics and treatment. Curr. Opin. Neurol. 14, 539–351.PubMedCrossRefGoogle Scholar
  19. Dirksen R. T. (2002) Bi-directional coupling between dihydropyridine receptors and ryanodine receptors. Front. Biosci. 7, d659-d670.PubMedCrossRefGoogle Scholar
  20. Doering C. J. and Zamponi G. W. (2003) Molecular pharmacology of high voltage-activated calcium channels. J. Bioenerg Biomembr. 35, 491–505.PubMedCrossRefGoogle Scholar
  21. Dolphin A. C. (2003) β subunits of voltage-gated calcium channels. J. Bioenerg. Biomembr. 35, 599–620.PubMedCrossRefGoogle Scholar
  22. Ertel E. A., Campbell K. P., Harpold M. M., et al. (2000) Nomenclature of voltage-gated calcium channels. Neuron 25, 533–535.PubMedCrossRefGoogle Scholar
  23. Felix R. (1999) Voltage-dependent Ca2+ channel α2δ auxieiary subunit: structure, function and regulation. Receptor Channel 6, 351–362.Google Scholar
  24. Felix R. (2000) Channelopathies: ion channel defects linked to heritable clinical disorders. J. Med. Genet. 57, 729–740.CrossRefGoogle Scholar
  25. Felix, R. (2002) In sights from mouse models of absence epilepsy into Ca2+ channel physiology and disease efiology. Cell Mol. Neurobiol. 22, 103–120.PubMedCrossRefGoogle Scholar
  26. Fontame B., Vale-Santos J., Jurkat-Rott K., et al. (1994) Mapping of the hypokalaemic periodic paralysis (HypoPP) locus to chromosome 1q31–32 in three European families. Nat. Genet. 6, 267–272.CrossRefGoogle Scholar
  27. Friend K. L., Crimmins D., Phan T. G., et al. (1999) Detection of a novel missense mutation and second recurrent mutation in the CACNA1A gene in individuals with EA-2 and FHM. Hum. Genet. 105, 261–265.PubMedCrossRefGoogle Scholar
  28. Geschwind D. H., Perlman S., Figueroa C. P., Treiman L. J., and Pulst S. M. (1997) The prevalence and wide clinical spectrum of the spinocerebellar ataxia type 2 trinucleotide repeat in patients with autosomal dominant cerebellar ataxia. Am. J. Hum. Genet. 60, 842–850.PubMedGoogle Scholar
  29. Grafe P., Quasthoff S., Strupp M., and Lehmann-Horn F. (1990) Enhancement of K+ conductance improves in vitro the contraction force of skeletal muscle in hypokalemic, periodic paralysis. Muscle Nerve 13, 451–457.PubMedCrossRefGoogle Scholar
  30. Griggs R. C., Moxley R. T. 3rd., Lafrance R. A., and McQuillen J. (1978) Hereditary paroxysmal ataxia: response to acetazolamide. Neurology 28, 1259–1264.PubMedGoogle Scholar
  31. Guida S., Trettel F., Pagnutti S., et al. (2001) Complete loss of P/Q calcium channel activity caused by a CACNA1A missense mutation carried by patients with episodic ataxia type 2. Am. J. Hum. Genet. 68, 759–764.PubMedCrossRefGoogle Scholar
  32. Hille B. (2001) Ion channels of excitable membranes. 3rd ed., Sinauer Associates Inc. Sunderland, MA.Google Scholar
  33. Iles D. E., Lehmann-Horn F., Scherer S. W., et al (1994). Localization of the gene encoding the α2/δ-subunits of the L-type voltage-dependent calcium channel to chromosome 7q and analysis of the segregation of flanking markers in malignant hyperthermia sus ceptible families. Hum. Mol. Genet. 3, 969–975.PubMedCrossRefGoogle Scholar
  34. Ishikawa K., Fujigasaki H., Saegusa H., et al. (1999) Abundant expression and cytoplasmic aggregations of α1A voltage-dependent calcium channel protein associated with neurodegeneration in spinocerebellar ataxia type 6. Hum. Mol. Genet. 8, 1185–1193.PubMedCrossRefGoogle Scholar
  35. Ishikawa K., Tanaka H., Saito M., et al. (1997) Japanese families with autosomal dominant pure cerebellar ataxia map to chromosome 19p13.1–p13.2 and are strongly associated with mild CAG expansions in the spinocerebellar ataxia type 6 gene in chromosome 19p13.1. Am. J. Hum. Genet. 61, 336–346.PubMedCrossRefGoogle Scholar
  36. Jacobi F. K., Hamel C. P., Arnaud B., et al. (2003) A novel CACNA1F mutation in a french family with the incomplete type of X-linked congenital stationary night blindness. Am. J. Ophthalmol. 135, 733–736.PubMedCrossRefGoogle Scholar
  37. Jen J., Wan J., Graves M., et al. (2001) Loss-of-function EA2 mutations are associated with impaired neuromuscular transmission. Neurology 57, 1843–1848.PubMedGoogle Scholar
  38. Jen J., Yue Q., Nelson S. F., et al. (1999) A novel nonsense mutation in CACNA1A causes episodic ataxia and hemiplegia. Neurology 53, 34–37.PubMedGoogle Scholar
  39. Jodice C., Mantuano E., Veneziano L., et al. (1997) Episodic ataxia type 2 (EA2) and spinocerebellar ataxia type 6 (SCA6) due to CAG repeat expansion in the CACNA1A gene on chromosome 19P. Hum. Mol. Genet. 6, 1973–1978.PubMedCrossRefGoogle Scholar
  40. Jun K., Piedras-Renteria E. S., Smith S. M., et al. (1999) Ablation of P/Q-type Ca2+ channel currents altered synaptic transmission, and progressive ataxia in mice lacking the α1-subunit. Proc. Natl. Acad. Sci. USA 96, 15,245–15,250.CrossRefGoogle Scholar
  41. Jurkat-Rott K., Lerche H., and Lehmann-Horn F. (2002) Skeletal muscle channelopathies. J. Neurol. 249, 1493–1502.PubMedCrossRefGoogle Scholar
  42. Kaja S., van de Ven R. C., Broos L. A., et al. (2005) Gene dosage-dependent transmitter release changes at neuromuscular synapses of CACNA1A R192Q knockin mice are non-progressive and do not lead to morphological changes or muscle weakness. Neuroscience 135, 81–95.PubMedCrossRefGoogle Scholar
  43. Kang M. G., Chen C. C., Felix R., et al. (2001) Biochemical and biophysical evidence for β2 subunit association with neuronal voltage-activated Ca2+ channels. J. Biol. Chem. 276, 32,917–32,924.Google Scholar
  44. Kang M. G. and Campbell K. P. (2003) Gamma subunit of voltage-activated calcium channels. J. Biol. Chem. 278, 21,315–21,318.Google Scholar
  45. Klugbauer N., Marais E., and Hofmann F. (2003) Calcium channel α2δ subunis: Differential expression, function, and drug binding. J. Bioenerg. Biomembr. 35, 639–647.PubMedCrossRefGoogle Scholar
  46. Kraus R.L., Sinnegger M. J., Glossmann H., Hering S., and Striessnig J. (1998) Familial hemiplegic migraine mutations change α1A Ca2+ channel kinetics. J. Biol. Chem. 273, 5586–5590.PubMedCrossRefGoogle Scholar
  47. Lacinovia L. (2005) Voltage-dependent calcium channels. Gen. Physiol. Biophys. 24(Suppl 1), 1–78.Google Scholar
  48. Lupie P., Goudet C., Nargeot J., Fontaine B., and Lory P. (1996) Electrophysiological properties of the hypokalaemic periodic paralysis mutation (R528H) of the skeletal muscle α1S subunit as expressed in mouse L cells. FEBS Lett. 382, 244–248.PubMedCrossRefGoogle Scholar
  49. Lorenzon N. M. and Beam K. G. (2000) Calcium channelopathies. Kidney Int. 57, 794–802.PubMedCrossRefGoogle Scholar
  50. MacLennan D. H., Phillips M. S., and Zhang Y. (1996) The genetic and physiological basis of malignant hyperthermia. in Molecular Biology of Membrane Transport Disorders, 2nd ed., Schultz S. G., Andreoli T. E., Brown A. M., Fambrough D. M., Hoffman J. F., and Welsh M. J., eds., Plenum Press, New York.Google Scholar
  51. Maselli R. A., Books W., and Dunne V. (2003) Effect of inherited abnormalities of calcium regulation on human neuromuscular transmission. Ann. NY Acad. Sci. 998, 18–28.PubMedCrossRefGoogle Scholar
  52. Matsuyama Z., Wakamori M., Mori Y., Kawakami H., Nakamura S., and Imoto K. (1999) Direct alteration of the P/Q-type Ca2+ channel property by polygfutamine expansion in spinocerebellar ataxia 6. J. Neurosci. 19, RC14:1–5.Google Scholar
  53. Matsuyama Z., Kawakami H., Maruyama H., et al. (1997) Molecular features of the CAG repeats of spinocerebellar ataxia 6 (SCA6). Hum. Mol. Genet. 6, 1283–1287.PubMedCrossRefGoogle Scholar
  54. Monnier N., Procaccio V., Stieglitz P., and Lunardi J. (1997) Malignant-hyperthermia susceptibility is associated with a mutation of the α1-subunit of the human dihydropyridine-sensitive L-type voltage-dependent calcium-channel receptor in skeletal muscle. Am. J. Hum. Genet. 60, 1316–1325.PubMedCrossRefGoogle Scholar
  55. Monnier N., Krivosic-Horber R., Payen J. F., et al. (2002) Presence of two different genetic traits in malignanthyperthermia families: implication for genetic analysis, diagnosis, and incidence of malignant hyperthermia susceptibility. Anethestiology 97, 1067–1074.CrossRefGoogle Scholar
  56. Monnier N., Romero N. B., Lerale J., et al. (2000) An autosomal dominant congenital myopathy with cores and rods is associated with a neomutation in the RYR1 gene encoding the skeletal muscle ryanodine receptor. Hum. Mol. Genet. 9, 2599–2608.PubMedCrossRefGoogle Scholar
  57. Morgans C. W., Gaughwin P., and Maleszka R. (2001) Expression of the α1F calcium channel subunit by photoreceptors in the rat retina. Mol. Vis. 7, 202–209.PubMedGoogle Scholar
  58. Morrill J. A. and Cannon S. C. (1999) Effects of mutations causing hypokalaemic periodic paralysis on the skeletal muscle L-type Ca2+ channel, expressed in Xenopus laevis oocytes. J. Physiol. (Lond.) 520(Part 2), 321–336.CrossRefGoogle Scholar
  59. Morrill J. A., Brown R. H. Jr., and Cannon S. C. (1998) Gating of the L-type Ca channel in human skeletal myotubes: an activation defect caused by the hypokalemic periodic paralysis mutation R528H. J. Neurosci. 18, 10,320–10,334.Google Scholar
  60. Nechiporuk T., Huynh D. P., Figueroa K., Sahba S., Nechiporuk A., and Pulst S. M. (1998) The mouse SCA2 gene: cDNA sequence, alternative splicing and protein expression. Hum Mol. Genet. 7, 1301–1309.PubMedCrossRefGoogle Scholar
  61. Ng T. M., Kohli A., Fagan S. C. Mohamed A. E., and Geiszt G. (2000) The effect of intravenous verapamil on cerebral hemodynamics in a migraine patient with hemiplegia. Ann. Pharmacother. 34, 39–43.PubMedCrossRefGoogle Scholar
  62. Ophoff R. A., Terwindt G. M., Vergouwe M. N., et al. (1996) Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the Ca2+ channel gene CACNL1A4. Cell 87, 543–552.PubMedCrossRefGoogle Scholar
  63. Piedras-Renteria E. S., Watase K., Harata N., et al. (2001) Increased expression of α1A Ca2+ channel currents arising from expanded trinucleotide repeats in spinocerebellar ataxia type 6. J. Neurosci. 21, 9185–9193.PubMedGoogle Scholar
  64. Pietrobon D. (2005a) Function and dysfunction of synaptic calcium channels: insights from mouse models. Curr. Opin. Neurobiol. 15, 257–265.PubMedCrossRefGoogle Scholar
  65. Pietrobon D. (2005b) Migraine: new molecular mechanisms. Neuroscientist 11, 373–386.PubMedCrossRefGoogle Scholar
  66. Prod'hom B., Pietrobon D., and Hess P. (1987) Direct measurement of proton transfer rates to a group controlling the dihydropyridine-sensitive Ca2+ channel. Nature 329, 243–246.PubMedCrossRefGoogle Scholar
  67. Ptacek L. J., Tawil R., Griggs R. C., et al. (1994) Dihydropyridine receptor mutations cause hypokalemic periodic paralysis. Cell 77, 863–868.PubMedCrossRefGoogle Scholar
  68. Pulst S. M., Nechiporuk A., Nechiporuk T., et al. (1996) Moderate expansion of a normally biallelic trinucleotide repeat in spincocerebellar ataxia type 2. Nat. Genet. 14, 269–276.PubMedCrossRefGoogle Scholar
  69. Pulst S. M., Santos N., Wang D., et al. (2005) Spinocerebellar ataxia type 2: polyQ repeat variation in the CACNA1A calcium channel modifies age of onset. Brain 128, 2297–2303.PubMedCrossRefGoogle Scholar
  70. Restimito, S., Thompson R. M., Eliet J., et al. (2000) The polyglutamine expansion in spinocerebellar ataxia type 6 causes a β-subunit-specific enhanced activation of P/Q-type calcium channels in Xenopus cocytes. J. Neurosci. 20, 6394–6403.Google Scholar
  71. Rios E. and Brum G. (1987) Involvement of dihydropyridine receptors in excitation-contraction coupling in skeletal muscle. Nature 325, 717–720.PubMedCrossRefGoogle Scholar
  72. Robinson R., Hopkins P., Carsana A., et al. (2003) Several interacting genes influence the malignant hyperthermiaphenotype. Hum. Genet. 112, 217, 218.PubMedGoogle Scholar
  73. Robinson R. L., Monnier N., Wolz W., et al. (1997) A genome wide search for susceptibility loci in three European malignant hyperthermia pedigrees. Hum. Mol. Genet. 6, 953–961.PubMedCrossRefGoogle Scholar
  74. Sasaki H., Kojima H., Yabe I., et al. (1998) Neuropathological and molecular studies of spincocerebellar ataxia type 6 (SCA6). Acta Neuropathol. 95, 199–204.PubMedCrossRefGoogle Scholar
  75. Schleithoff L., Mehrke G., Reutlinger B., and Lehmann-Horn F. (1999) Genomic structure and functional expression of a human α2/δ calcium channel subunit gene (CACNA2). Genomics 61, 201–209.PubMedCrossRefGoogle Scholar
  76. Silver K. and Andermann F. (1993) Alternating hemiplegia of childhood: a study of 10 patients and results of flunarizine treatment. Neurology 43, 36–41.PubMedGoogle Scholar
  77. Sipos I., Jurkat-Rott K., Harasztosi C., et al. (1995) Skeletal muscle DHP receptor mutations after calcium currents in human hypokalaemic periodic paralysis myotubes. J. Physiol. 483 (Part 2), 299–306.PubMedGoogle Scholar
  78. Scancey S. D., Hildebrand M. E., Materek L. A., Bird T. D., and Snutch T. P. (2004) Functional implications of a novel EA2 mutation in the P/Q-type calcium channel. Ann. Neurol. 56, 213–220.CrossRefGoogle Scholar
  79. Stewart S. L., Hogan K., Rosenberg H., and Fletcher J. E. (2001) Identification of the Arg1086His mutation in the alpha subunit of the voltage-dependent calcium channel (CACNA1S) in a North American family with malignant hyperthermia. Clin. Genet. 59, 178–184.PubMedCrossRefGoogle Scholar
  80. Striessnig J., Hoda J. C., Koschak A., et al. (2004) L-type Ca2+ channels in Ca2+ channelopathies. Biochem. Biophys. Res. Commun. 322, 1341–1346.PubMedCrossRefGoogle Scholar
  81. Strom T. M., Nyakatura G., Apfelstedt-Sylla, E., et al. (1998) An L-type calcium-channel gene mutated in incomplete X-linked congenital stationary right blindness. Nat. Genet. 19, 260–263.PubMedCrossRefGoogle Scholar
  82. Takano H., Cancel G., Ikeuchi T., et al. (1998) Close associations between prevalences of dominantly inherited spinocerebellar ataxias with CAG repeat expansions and frequencies of large normal CAG alleles in Japanese and Caucasian populations. Am. J. Hum. Genet. 63, 1060–1066.PubMedCrossRefGoogle Scholar
  83. Tawil R., McDermott M. P., Brown R. Jr., et al. (2000) Randomized trials of dichlorphenamide in the periodic paralyses. Working Group on Periodic Paralysis. Ann. Neurol. 47, 46–53.PubMedCrossRefGoogle Scholar
  84. Toru S., Murakoshi T., Ishikawa K., et al. (2000) Spinocerebellar ataxia type 6 mutation alters P-type calcium channel function. J. Biol. Chem. 275, 10,893–10,898.CrossRefGoogle Scholar
  85. Tricarico D., Servidei S., Tonali P., Jurkat-Rott K., and Camerino D. C. (1999) Impairment of skeletal muscle adenosine triphosphate-sensitive K+ chainnels in patients with hypokalemic periodic paralysis. J. Clin. Invest. 103, 675–682.PubMedCrossRefGoogle Scholar
  86. van den Maagdenberg A. M., Kors, E. E., Brunt E. R., et al. (2002) Episodic ataxia type 2. Three novel truncating mutations and one novel missense mutation in the CACNA1A gene. J. Neurol. 249, 1515–1519.PubMedCrossRefGoogle Scholar
  87. van den Maagdenberg A. M., Pietrobon D., Pizzorusso T., et al. (2004) A Cacnala knockin migraine mouse model with increased susceptibility to cortical spreading depression. Neuron 41, 701–710.PubMedCrossRefGoogle Scholar
  88. Varadi G., Mori Y., Mikala G., and Schwartz A. (1995) Molecular determinants of Ca2+ channel function and drug action. Trends Pharmacol. Sci. 16, 43–49.PubMedCrossRefGoogle Scholar
  89. Walker D. and De Waard M. (1998) Subunit interaction sites in voltage-dependent Ca2+ channel strole in channel function. Trends Neurosci. 21, 148–154.PubMedCrossRefGoogle Scholar
  90. Wappl E., Koschak A., Poteser M., et al. (2002) Functional consequences of P/Q type Ca2+ channel Cav2.1 missense mutations associated with episodic ataxia type 2 and progressive ataxia. J. Biol. Chem. 277, 6960–6966.PubMedCrossRefGoogle Scholar
  91. Weiss R. G., O'Connell K. M., Flucher B. E., Allen P. D., Grabner M., and Dirksen R. T. (2004) Functional analysis of the R1086H malignant hyperthermia mutation in the DHPR reveals an unexpected influence of the III–IV loop on skeletal muscle EC coupling. Am. J. Physiol. Cell Physiol. 287, C1094-C1102.PubMedCrossRefGoogle Scholar
  92. Yu W. and Horowitz S. H. (2003) Treatment of sporadic hemiplegimigraine with calcium-channel blocker verapamil. Neurology 60, 120, 121.PubMedGoogle Scholar
  93. Zhuchenko O., Bailey J., Bonnen P., et al. (1997) Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the α1A-voltage-dependent calcium channel. Nat. Genet. 15, 62–69.PubMedCrossRefGoogle Scholar

Copyright information

© Humana Press Inc. 2006

Authors and Affiliations

  1. 1.Department of Cell Biology, Center for Research and Advanced StudiesNational Polytechnic Institute (Cinvestav-IPN)Mexico CityMexico

Personalised recommendations