Lack of effect of miller fisher sera/plasmas on transmitter release from PC12 cells

Michael G. Benatar, Hugh J. Willison, Angela Vincent

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

IgG antibodies to GQ(1b) ganglioside are found in > 90% of patients with the Miller Fisher Syndrome (MFS). MFS sera or IgG preparations have marked effects on neurotransmitter release at the neuromuscular junction but their mode(s) of action remain unclear. To establish a cell-based system for investigating the mechanism of action of MFS serum preparations, we looked at neurotransmitter release from three cell lines. We failed to demonstrate substantial 14C-acetylcholine release from two motor-neuronal cell lines, VSC4.1 and NSC19 and therefore studied 3H-noradrenaline release from NGF- differentiated PC12 cells a neural-crest derived catecholaminergic cell line. K+-induced release was inhibited by botulinum toxin and basal release was enhanced by α-latrotoxin, resembling that at the neuromuscular junction, although K+-induced release was dependent on L-type rather than P/Q-type calcium channels. The cells expressed polysialylated gangliosides on the cell surface. Incubation in hear-inactivated or untreated MFS preparations did not, however, affect basal or K+-induced release. Thus the PC12 cells do not appear to be sensitive to the effects of serum antibodies from MFS patients.

Original languageEnglish (US)
Pages (from-to)1-5
Number of pages5
JournalJournal of Neuroimmunology
Volume80
Issue number1-2
DOIs
StatePublished - Dec 1997
Externally publishedYes

Keywords

  • Ganglioside GQ(1b)
  • Miller Fisher
  • NSC19
  • PC12 Cells
  • VSC4.1

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

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