LOGIN TO YOUR ACCOUNT

Username
Password
Remember Me
Or use your Academic/Social account:

CREATE AN ACCOUNT

Or use your Academic/Social account:

Congratulations!

You have just completed your registration at OpenAire.

Before you can login to the site, you will need to activate your account. An e-mail will be sent to you with the proper instructions.

Important!

Please note that this site is currently undergoing Beta testing.
Any new content you create is not guaranteed to be present to the final version of the site upon release.

Thank you for your patience,
OpenAire Dev Team.

Close This Message

CREATE AN ACCOUNT

Name:
Username:
Password:
Verify Password:
E-mail:
Verify E-mail:
*All Fields Are Required.
Please Verify You Are Human:
fbtwitterlinkedinvimeoflicker grey 14rssslideshare1
Languages: English
Types: Article
Subjects:
Identifiers:doi:10.1002/syn.20747
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 Cav2.1 channels, affecting the magnitude and kinetics of the Ca2+ 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.
  • The results below are discovered through our pilot algorithms. Let us know how we are doing!

    • Bullens RW, O'Hanlon GM, Wagner E, Molenaar PC, Furukawa K, Furukawa K, Plomp JJ, Willison HJ. 2002. Complex gangliosides at the neuromuscular junction are membrane Inoue M, Fujii Y, Furukawa K, Okada M, Okumura K, Hayakawa T, Furukawa K, Sugiura Y. 2002. Refractory skin injury in complex knock-out mice expressing only the GM3 ganglioside. J Biol Chem 277:29881-29888.
    • Isaev D, Isaeva E, Shatskih T, Zhao Q, Smits NC, Shworak NW, Khazipov R, Holmes GL. 2007. Role of extracellular sialic acid in regulation of neuronal and network excitability in the rat hippocampus. J Neurosci 27:11587-11594.
    • Kaja S, van de Ven RC, Broos LA, Frants RR, Ferrari MD, van den Maagdenberg AM, Plomp JJ. 2007. Characterization of acetylcholine release and the compensatory contribution of non-Ca(v)2.1 channels at motor nerve terminals of leaner Ca(v)2.1-mutant mice. Neuroscience 144:1278-1287.
  • No related research data.
  • No similar publications.

Share - Bookmark

Download from

Funded by projects

Cite this article