Increase of GQ1b in the hippocampus of mice following kindled-seizures

Neurosci Lett. 2008 Aug 29;441(3):286-90. doi: 10.1016/j.neulet.2008.06.058. Epub 2008 Jun 26.

Abstract

The ganglioside GQ1b facilitates the influx of Ca2+ in brain synaptosomes and enhances ATP-induced long-term potentiation in hippocampal slices. Anti-GQ1b antibody impairs the function of peripheral neurons, for example, it had pathogenic effects on presynaptic neuronal membranes and perisynaptic Schwann cells in a mouse model of Guillain-Barré syndrome. The present study demonstrated in vivo that the level of endogenous GQ1b was relevant to neural function in the brain, in that it increased following seizures in amygdaloid kindling mice. GQ1b is subject to epileptogenic regulation and may play a role in the development of epilepsy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amygdala / metabolism
  • Amygdala / physiopathology
  • Animals
  • Disease Models, Animal
  • Epilepsy / genetics
  • Epilepsy / metabolism*
  • Epilepsy / physiopathology
  • Gangliosides / metabolism*
  • Growth Cones / metabolism
  • Hippocampus / metabolism*
  • Kindling, Neurologic / genetics
  • Kindling, Neurologic / metabolism*
  • Lipid Metabolism / physiology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Nerve Fibers, Myelinated / metabolism
  • Neuronal Plasticity / physiology
  • Neurons / metabolism
  • Up-Regulation*

Substances

  • Gangliosides
  • GQ1b ganglioside