The role of sialic acid in the nerve terminal for the release of transmitter.
The role of sialic acid in the frequency of miniature endplate potentials (MEPPs) was examined using neuraminidase and gangliosides in the mouse diaphragm. Neuraminidase increased and decreased MEPP frequency in normal K+ and high K+ solution, respectively. The effects were dependent on the presence of Ca2+ in extracellular medium. Neuraminidase liberated sialic acid from and lowered Ca2+-binding capacity of synaptosomal membrane. Gangliosides treatment of the tissue partially restored the effects of neuraminidase on the frequency of MEPP and Ca2+-binding capacity. It is possible that sialic acid in the nerve endings provides a functional storage site which supply intracellular Ca2+ to cause a transmitter release.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D003964:Diaphragm; D005732:Gangliosides / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009045:Motor Endplate / Q000187:drug effects / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D009439:Neuraminidase / Q000494:pharmacology; D009469:Neuromuscular Junction / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D012794:Sialic Acids / Q000502:physiology*; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism
D005732:Gangliosides; D018377:Neurotransmitter Agents; D012794:Sialic Acids; D009439:Neuraminidase; D008274:Magnesium; D011188:Potassium; D002118:Calcium