Article
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 - 23 Feb 2007
Kaja S, van de Ven R C G, Broos L A M, Frants R R, Ferrari M D, van den Maagdenberg A M J M, Plomp J J
Abstract excerpt
The severely ataxic and epileptic mouse leaner (Ln) carries a natural splice site mutation in Cacna1a, leading to a C-terminal truncation of the encoded Ca(v)2.1 alpha(1) protein. Ca(v)2.1 is a neuronal Ca(2+) channel, mediating neurotransmitter release at many central synapses and the peripheral neuromuscular junction (NMJ). With electrophysiological analyses we demonstrate severely reduced ( approximately 50%)...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.