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Anti-ganglioside antibodies alter presynaptic release and calcium influx.

Anti-ganglioside antibodies alter presynaptic release and calcium influx. Research Abstract Details 

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  • Anti-ganglioside antibodies alter presynaptic release and calcium influx. Abstract Text:

    brigitte buchwaldBrigitte Buchwald,gang zhangGang Zhang,angela k vogt-eiseleAngela K Vogt-Eisele,weiyi zhangWeiyi Zhang,raheleh ahangariRaheleh Ahangari,john w griffinJohn W Griffin,hanns hattHanns Hatt,klaus v toykaKlaus V Toyka,kazim a sheikhKazim A Sheikh,brigitte buchwaldBrigitte Buchwald,gang zhangGang Zhang,angela k vogt-eiseleAngela K Vogt-Eisele,weiyi zhangWeiyi Zhang,raheleh ahangariRaheleh Ahangari,john w griffinJohn W Griffin,hanns hattHanns Hatt,klaus v toykaKlaus V Toyka,kazim a sheikhKazim A Sheikh,

    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-ganglioside 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.

    Anti-ganglioside antibodies alter presynaptic release and calcium influx. Publishing Authors By Initials

    b buchwaldB Buchwald,g zhangG Zhang,ak vogt-eiseleAK Vogt-Eisele,w zhangW Zhang,r ahangariR Ahangari,jw griffinJW Griffin,h hattH Hatt,kv toykaKV Toyka,ka sheikhKA Sheikh,b buchwaldB Buchwald,g zhangG Zhang,ak vogt-eiseleAK Vogt-Eisele,w zhangW Zhang,r ahangariR Ahangari,jw griffinJW Griffin,h hattH Hatt,kv toykaKV Toyka,ka sheikhKA Sheikh,

    For similar abstracts research abstracts see: abstracts research

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    Anti-ganglioside antibodies alter presynaptic release and calcium influx. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Neurobiology of disease

    VOLUME: 28

    Page Numbers: 113-21

    Journal Abbreviation: Neurobiol. Dis.

    ISSN: 0969-9961

    DAY: 14

    MONTH: 07

    YEAR: 2007

    Anti-ganglioside antibodies alter presynaptic release and calcium influx. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9500169

    Anti-ganglioside antibodies alter presynaptic release and calcium influx. Keywords Mesh Terms:

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    Grant and Affiliation Information for Anti-ganglioside antibodies alter presynaptic release and calcium influx.

    AFFILIATION: Research Group Neurophysiology, Section Neurology, Max-Planck-Institute of Psychiatry, Munich, Germany.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS54962

    ACRONYM: NS

    MEDLINETA: Neurobiol Dis

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