Homeostatic compensation maintains Ca2+ signaling functions in Purkinje neurons in the leaner mutant mouse

被引：18

作者：

Murchison D. ^{[1
]}

Dove L.S. ^{[2
]}

Abbott L.C. ^{[3
]}

Griffith W.H. ^{[1
]}

机构：

[1] Department of Medical Pharmacology and Toxicology, College of Medicine, Texas A and M University System Health Science Center, College Station

[2] PPD Development, Austin, TX

[3] Department of Veterinary Anatomy and Public Health, College of Veterinary Medicine, Texas A and M University, College Station, TX

来源：

The Cerebellum | 2002年 / 1卷 / 2期

关键词：

Ca [!sup]2+[!/sup] binding protein; Ca[!sup]2+[!/sup] buffering; Mutant mice; Voltage-gated Ca[!sup]2+[!/sup] channels;

D O I：

10.1080/147342202753671259

中图分类号：

学科分类号：

摘要：

Several human neurological disorders have been associated with mutations in the gene coding for the al subunit of the P/Q type voltage-gated calcium channel (α1A/CaV2.1). Mutations in this gene also occur in a number of neurologically afflected mouse strains, including leaner (tg1a/tg1a). Because the P-type calcium current is very prominent in cerebellar Purkinje neurons, these cells from mice with α1 subunit mutations make excellent models for the investigation of the functional consequences of native mutations in a voltage-gated calcium channel of mammalian central nervous system. In this review, we describe the impact of altered channel function on cellular calcium homeostasis and signaling. Remarkably, calcium buffering functions of the endoplasmic reticulum and calcium-binding proteins appear to be regulated in order to compensate for altered calcium influx through the mutant channels. Although this compensation may serve to maintain calcium signaling functions, such as calcium-induced calcium release, it remains uncertain whether such compensation alleviates or contributes to the behavioral phenotype. © 2002 Martin Dunitz Ltd.

引用

页码：119 / 127

页数：8

共 68 条

[31]

Tse A., Tse F.W., Hille B., Calcium homeostasis in identified rat gonadotrophs, J Physiol (Lond), 477, pp. 511-525, (1994)

[32]

Grynkiewicz G., Poenie M., Tsien R.Y., A new generation of calcium indicators with greatly improved fluorescence properties, J Biol Chem, 260, pp. 3440-3450, (1985)

[33]

Verkhratsky A., Shmigol A., Calcium-induced calcium release in neurons, Cell Calcium, 19, pp. 1-14, (1996)

[34]

Brorson J.R., Bleakman D., Gibbons S.J., Miller R.J., The properties of intracellular calcium stores in cultured rat cerebellar neurons, J Neurosci, 11, pp. 4024-4043, (1991)

[35]

Berridge M.J., Neuronal calcium signaling, Neuron, 21, pp. 13-26, (1998)

[36]

Isaacs K.R., Abbott L.C., Development of the paramedian lobule of the cerebellum in wild-type and tottering mice, Devel Neurosci, 14, pp. 386-393, (1992)

[37]

Inoue T., Lin X., Kohlmeier K.A., Orr H.T., Zoghbi H.Y., Calcium dynamics and electrophysiological properties of cerebellar Purkinje cells in SCA1 transgenic mice, J Neurophysiol, 85, pp. 1750-1760, (2001)

[38]

Vig P.J.S., Subramony S.H., Burright E.N., Fratkin J.D., McDaniel D.O., Desaiah D., Qin Z., Reduced immunoreactivity to calcium-binding proteins in Purkinje cells precedes onset of ataxia in spinocerebellar ataxia-1 transgenic mice, Neurology, 50, pp. 106-113, (1998)

[39]

Kaemmerer W.F., Rodrigues C.M.P., Steer C.J., Low W.C., Creatine-supplemented diet extends Purkinje cell survival in spinocerebellar ataxia type1 transgenic mice but does not prevent the ataxic phenotype, Neuroscience, 103, pp. 713-724, (2001)

[40]

Mullen R.J., Eicher E.M., Sidman R.L., Purkinje cell degeneration, a new mutation in the mouse, Proc Natl Acad Sci USA, 73, pp. 208-212, (1976)

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