Axons and multiple sclerosis

Multiple Sclerosis

Volumn 15, Issue 2, 2009, Pages 278-

  Alix, James J P ^a  

^a IMPERIAL COLLEGE LONDON   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

SODIUM CHANNEL; VOLTAGE GATED CALCIUM CHANNEL;

CALCIUM TRANSPORT; DEMYELINATION; HUMAN; LETTER; METABOLIC STRESS; MULTIPLE SCLEROSIS; NERVE CELL MEMBRANE STEADY POTENTIAL; NERVE FIBER; NERVE POTENTIAL; NEUROPATHOLOGY; PATHOPHYSIOLOGY; PROTEIN EXPRESSION; SODIUM TRANSPORT; SYNAPTIC TRANSMISSION;

AXONS; HUMANS; MULTIPLE SCLEROSIS; NERVE DEGENERATION;

EID: 59349089207     PISSN: 13524585     EISSN: None     Source Type: Journal    
DOI: 10.1177/1352458508099140     Document Type: Letter

References (5)

1. Wilkins A, Scolding N. Protecting axons in multiple sclerosis. Mult Scler 2008; 14: 1013-1025.
2. Alix JJ, Dolphin AC, Fern R. Vesicular apparatus, including functional calcium channels, are present in developing rodent optic nerve axons and are required for normal node of Ranvier formation. J Physiol 2008; 586: 4069-4089.
3. Kukley M, Capetillo-Zarate E, Dietrich D. Vesicular glutamate release from axons in white matter. Nat Neurosci 2007; 10: 311-320.
4. Ziskin JL, Nishiyama A, Rubio M, Fukaya M, Bergles DE. Vesicular release of glutamate from unmyelinated axons in white matter. Nat Neurosci 2007; 10: 321-330.
5. Kornek B, Storch MK, Bauer J. Distribution of a calcium channel subunit in dystrophic axons in multiple sclerosis and experimental autoimmune encephalomyelitis. Brain 2001; 124: 1114-1124.