Anti-ganglio side antibodies alter presynaptic release and calcium influx

作者：Buchwald Brigitte; Zhang Gang; Vogt Eisele Angela K; Zhang Weiyi; Ahangari Raheleh; Griffin John W; Hatt Hanns; Toyka Klaus V; Sheikh Kazim A^*

来源：Neurobiology of Disease, 2007, 28(1): 113-121.

DOI：10.1016/j.nbd.2007.07.008

• Guillain-Barre syndrome
• AMAN
• anti-ganglioside antibodies
• gangliosides
• immune neuropathies
• neuromuscular junction
• calcium influx

Acute motor axonal neuropathy (AMAN) variant of Guillain-Barr 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 -GD1 a 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.

• 出版日期2007-10
• 单位河北医科大学