Autoantibodies in Neurological Diseases by G. Martino, A. Vincent (auth.), Angela Vincent, Gianvito

By G. Martino, A. Vincent (auth.), Angela Vincent, Gianvito Martino (eds.)

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Extra resources for Autoantibodies in Neurological Diseases

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Am J Med Genet Mar 6:91:22-28 Pinto A, Gillard S, Moss F et al (1998) Human autoantibodies specific for the alA calcium channel subunit reduce both P-type and Q-type calcium currents in cerebellar neurons. Proc Natl Acad Sci USA 95:8328-8333 Trivedi R, Mundanthanam G,Amyes E et al (2000) Autoantibody screening in subacute cerebellar ataxia. Lancet 356:565-566 New Antibodies to Neuronal and Muscle Antigens 27 24. Hart IK (2000) Acquired neuromyotonia: a new autoantibody-mediated neuronal potassium channelopathy.

Not only the peripheral NMT but also the excessive secretions and itchy skin rash improved. However, after treatment, when he was well enough to undergo more extensive testing, there were marked abnormalities of diurnal levels of neuropeptides and hormones, with raised cortisol and norepinephrine levels and reduced levels and flattened circadian rhythms of prolactin and melatonin. Particularly intriguing was the fact that many of the clinical features of Morvan's disease and the changes in hormone and peptide levels were very similar to those previously reported in fatal familial insomnia (FFI), a genetic prion disease [28].

From [13], by permission channels are associated with cerebellar granule cells and hippocampal neurons [13]. Pharmacologically, both channels can be blocked by w-agatoxin IVA (P channels with high and Q channels with low affinity) and by w-conotoxin MVIIC [19]. The alA subunits which form both P and Q channels are thought to derive from the same gene, the different sensitivities to w-agatoxin IVA probably being due to the product of alternative mRNA splicing [13,14]. Neurotransmitter release from synaptic vesicles requires the influx of Ca2+ through VGCCs, and a marked and rapid rise in the intracellular Ca 2+ is required to trigger exocytosis.

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