| Autor: |
Brigitte Buchwald, Gang Zhang, Angela K. Vogt-Eisele, Weiyi Zhang, Raheleh Ahangari, John W. Griffin, Hanns Hatt, Klaus V. Toyka, Kazim A. Sheikh |
| Jazyk: |
angličtina |
| Rok vydání: |
2007 |
| Předmět: |
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| Zdroj: |
Neurobiology of Disease, Vol 28, Iss 1, Pp 113-121 (2007) |
| Druh dokumentu: |
article |
| ISSN: |
1095-953X |
| DOI: |
10.1016/j.nbd.2007.07.008 |
| Popis: |
Acute motor axonal neuropathy (AMAN) variant of Guillain–Barré syndrome is often associated with IgG anti-GM1 and -GD1a antibodies. The pathophysiological basis of antibody-mediated selective motor nerve dysfunction remains unclear. We investigated the effects of IgG anti-GM1 and -GD1a monoclonal antibodies (mAbs) on neuromuscular transmission and calcium influx in hemidiaphragm preparations and in cultured neurons, respectively, to elucidate mechanisms of Ab-mediated muscle weakness. Anti-GM1 and -GD1a mAbs depressed evoked quantal release to a significant yet different extent, without affecting postsynaptic currents. At equivalent concentrations, anti-GD1b, -GT1b, or sham mAbs did not affect neuromuscular transmission. At fourfold higher concentration, an anti-GD1b mAb (specificity described in immune sensory neuropathies) induced completely reversible blockade. In neuronal cultures, anti-GM1 and -GD1a mAbs significantly reduced depolarization-induced calcium influx. In conclusion, different anti-gangliosde mAbs induce distinct effects on presynaptic transmitter release by reducing calcium influx, suggesting that this is one mechanism of antibody-mediated muscle weakness in AMAN. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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