Neural control of the expression of a Ca2+-activated K+ channel involved in the induction of myotonic-like characteristics

Cellular and Molecular Neurobiology

Volumn 16, Issue 1, 1996, Pages 39-49

  Ramírez, Beatriz U ^a   Behrens, Maria Isabel ^b   Vergara, Cecilia ^c  

^a PONTIFICIA UNIVERSIDAD CATÓLICA DE CHILE   (Chile)

^b HOSPITAL DR SÓTERO DEL RÍO   (Chile)

^c UNIVERSITY OF CHILE   (Chile)

Author keywords

Apamin receptor; Axonal transport; Electrical activity; Myotonia

Indexed keywords

APAMIN; CALCIUM; COLCHICINE; IODINE 125; POTASSIUM; POTASSIUM CHANNEL; VINBLASTINE;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; EXTENSOR DIGITORUM LONGUS MUSCLE; MALE; MUSCLE DENERVATION; MUSCLE ISOMETRIC CONTRACTION; MUSCLE TWITCH; MYOTONIC DYSTROPHY; NERVE FIBER TRANSPORT; NERVE STIMULATION; NONHUMAN; PRIORITY JOURNAL; RAT; SCIATIC NERVE; TIBIALIS ANTERIOR MUSCLE;

ANIMALS; APAMIN; AXONAL TRANSPORT; COLCHICINE; GENE EXPRESSION; MALE; MUSCLE CONTRACTION; MUSCLE DENERVATION; MUSCLE, SKELETAL; MYOTONIC DYSTROPHY; POTASSIUM CHANNELS; RATS; RATS, SPRAGUE-DAWLEY; REFERENCE VALUES; SCIATIC NERVE; VINBLASTINE;

EID: 0030044626     PISSN: 02724340     EISSN: None     Source Type: Journal    
DOI: 10.1007/BF02578385     Document Type: Article

References (28)

1. Adrian, R. H., and Bryant, S. H. (1974). On the repetitive discharge in myotonic muscle fibers. J. Physiol. 240:505-515.
2. Barchi, R. L., and Furman, R. E. (1992). Pathophysiology of myotonia and periodic paralysis. In Asbury, A. K., McKhann, G. M., and McDonald, W. J. (Eds.); Diseases of the Nervous System; Clinical Neurobiology, W. B. Saunders, Philadelphia, Vol. 1, pp. 146-163.
3. Behrens, M. I., and Vergara, C. (1992). Increase of apamin receptors in skeletal muscle induced by colchicine: Possible role in myotonia. Am. J. Physiol. 263:C794-C802.
4. Behrens, M. I., Torrealba, G., Soza, M. A., Court, J., and Ramirez, B. U. (1983). Axonal transport dysfunction in dystrophia myotonica. Acta Neuropathol. 62:157-158.
5. + channels in myotonic dystrophy. Muscle Nerve 17:1264-1270.
6. Brook, J. D., McCurrach, M. E., Harley, H. G., Buckler, A. J., Church, D., Abuvatani, H., Hunter, K., Stanton, V. P., Thirion, J.-P., Hudson, T., Sohn, R., Zemelman, B., Snell, R. G., Rundle, S. A., Crow, S., Davies, J., Shelbourne, P., Buxton, J., Jones, C., Juronen, V., Johnson, K., Harper, P. S., Shaw, D. J., and Housman, D. E. (1992). Molecular basis of myotonic dystrophy: Expansion of a trinucleotide (CTG) repeat of the 3′ end of a transcript encoding a protein kinase family member. Cell 68:799-808.
7. Cannon, S. C. (1994). Slow sodium channel inactivation need not be disrupted in the pathogenesis of myotonia and periodic paralysis. Biophys. J. 66:543-544.
8. Cannon, S. C., Brown, R. H., and Corey, D. P. (1993). Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels. Biophys J. 65:270-288.
9. Chachine, M., George, A. L., Jr., Zhou, M., Ji, S., Sun, W., Barchi, R. L., and Horn, R. (1994). Sodium channel mutations in paramyotonia congenita uncouple inactivation from activation. Neuron 12:281-294.
10. - conductance in resealed muscle fibre segments from patients with myotonic dystrophy. J. Physiol 425:391-405.
11. Fu, Y.-H., Friedman, D. L., Richards, S., Pearlman, J. A., Gibbs, R. A., Pizzuti, A., Ashizawa, T., Ferryman, M. B., Scarlato, G., Fenwick, R. G., Jr., and Caskey, C. T. (1993). Decreased expression of myotonin-protein kinase messenger RNA and protein in adult form of myotonic dystrophy. Science 260:235-238.
12. Hall, Z. W., and Sanes, J. R. (1993). Synaptic structure and development: The neuromuscular junction. Neuron 10:99-121.
13. Hille, B. (1992). Ionic Channels of Excitable Membranes, Sinauer Associates, Sunderland, MA.
14. Huang, C. F., Neville, C. M., and Schmidt, J. (1993). Control of myogenic factor genes by the membrane depolarization/protein kinase C cascade in chick skeletal muscle. FEBS Lett. 319:21-25.
15. Hugues, M., Romey, G., Duval, D., Vincent, J. P., and Lazdunski, M. (1982). Apamin as a selective blocker of the calcium-dependent potassium channel in neuroblastoma cells: Voltage-clamp and biochemical characterization of the toxin receptor. Proc. Natl. Acad. Sci. 79:1308-1312.
16. Inestrosa, N. C., and Fernández, H. L. (1976). Muscle enzymatic changes induced by blockage of axoplasmic transport. J. Neurophysiol. 39:1236-1245.
17. Lomo, T., and Rosenthal, J. (1972). Control of the Ach sensitivity by muscle activity in the rat. J. Phys. 221:493-513.
18. Luco, J. V., and Eyzaguirre C. (1955). Fibrillation and hypersensitivity to Ach in denervated muscle: Effect of length of degenerating nerve fibers. J. Neurophys. 18:65-73.
19. Lupa, M. T., and Caldwell, J. H. (1994). Sodium channels aggregate at former synaptic sites in innervated and denervated regenerating muscles. J. Cell Biol. 124:139-147.
20. McManus, O. (1991). Ca-activated K channels: Regulation by calcium. L. Bioenerg. Biomembr. 23:561-576.
21. Mrak, R. E. (1985). In Muscle Membranes in Diseases of Muscle, CRC Press, Boca Raton, FL.
22. Ramírez, B. U. (1980). Neurotrophic regulation of muscle autolytic activity. Exp. Neurol. 67:257-264.
23. Renaud, J. F., Desnuelle, C., Schmid-Antomarchi, H., Hugues, M., Serratrice, G., and Lazdunski, M. (1986). Expression of apamin receptors in muscles of patients with myotonic muscular dystrophy. Nature 319:678-680.
24. Rudel, R., and Lehmann-Horn, F. (1985). Membrane changes in cells from myotonia patients. Physiol. Rev. 65:310-356.
25. Rudel, R. Ruppersberg, J. P., and Spittelmeister, W. (1989). Abnormalities of the fast sodium current in myotonic dystrophy, recessive generalized myotonia, and adynamia episodica. Muscle Nerve 12:281-287.
26. Sampson, S. R., and Alboim, S. V. (1993). Regulation of voltage-sensitive K-channels in cultured rat skeletal muscle. Soc. Neurosci. Abstr. 19:706.
27. + channel in mammalian skeletal muscle. Proc. Natl. Acad. Sci. USA 82:2188-2191.
28. Schuetze, S. M., and Role L. (1987). Developmental regulation of nicotinic acetylcholine receptors. Annu. Rev. Neurosci. 10:403-457.