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Total ganglioside ablation at mouse motor nerve terminals alters neurotransmitter release level
Author(s) -
Zitman Femke M.P.,
Todorov Boyan,
Furukawa Keiko,
Furukawa Koichi,
Willison Hugh J.,
Plomp Jaap J.
Publication year - 2010
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20747
Subject(s) - neurotransmitter , neuromuscular junction , neurotransmission , acetylcholine , neuromuscular transmission , motor nerve , chemistry , synaptic vesicle , stimulation , ganglioside , neuroscience , biophysics , electrophysiology , endocrinology , biology , biochemistry , membrane , receptor , vesicle
Abstract Neuronal membrane gangliosides, forming a large family of sialylated glycosphingolipids, have been hypothesized to play important roles in synaptic transmission. We studied the ex vivo electrophysiological function of neuromuscular junctions of GM2/GD2‐synthase*GD3‐synthase compound null ‐mutant mice after acute removal of GM3, the only remaining ganglioside in this mouse, by in vitro treatment with neuraminidase. We found 16% enhancement of the acetylcholine release per nerve impulse at low‐rate (0.3 Hz) nerve stimulation. Conversely, the treatment reduced the acetylcholine release evoked by high‐rate (40 Hz) nerve stimulation. Also, 25 ms paired‐pulse facilitation of endplate potentials was reduced by the neuraminidase‐treatment. These effects may indicate a modest modulatory influence of the negative electrical charges carried by the sialic acid molecules of gangliosides on the function of presynaptic Ca v 2.1 channels, affecting the magnitude and kinetics of the Ca 2+ influx that induces neurotransmitter release from the motor nerve terminal. Our results show that gangliosides are to some extent involved in neurotransmission at the neuromuscular junction, but that their presence is not an absolute requirement in this process. Synapse 64:335–338, 2010. © 2009 Wiley‐Liss, Inc.