Evidence for the functional role of monosialoganglioside GM1 in synaptic transmission in the rat hippocampus.

The hippocampal slices were incubated with compounds which hydrolyze, modify or bind with sialic acid containing molecules. The efficiency of synaptic transmission was tested in the presence of these compounds. The size of the evoked extracellularly recorded potential following Schaffer collateral stimulation was used as an indicator of synaptic transmission efficiency. Sodium periodate (10 mM) and sodium perchlorate (59.2 mM) evoked a reversible (after washout) decrease in the size of the population spike. Higher concentration of sodium periodate (60 mM) abolished the size of the population spike, which was only poorly reversible after washout. Tetanus toxin, which binds to polysialogangliosides, and neuraminidase from Vibrio cholerae (an enzyme which splits off sialic acid from polysialogangliosides, leaving GM1 intact, and splits off sialic acid from sialoglycoproteins) had no influence on the size of the population spike. Cholera toxin, which binds to GM1, slightly reduced the size of the population spike. Incubation of the slices with neuraminidase from Arthrobacter ureafaciens (an enzyme which splits off sialic acid from all gangliosides, including GM1, and from sialoglycoproteins) abolished the population spike after 5 h. GM1 antiserum abolished the potential after approximately 100 min. The conclusion is drawn that of all gangliosides only GM1 is necessary to support synaptic transmission in Schaffer collateral-pyramidal cell synapses.