Vesicular reuptake inhibition by a synaptotagmin I C2B domain antibody at the squid giant synapse
AUTOR(ES)
Llinás, Rodolfo R.
FONTE
National Academy of Sciences
RESUMO
Synaptotagmin (Syt) I, a ubiquitous synaptic vesicle protein, comprises a transmembrane region and two C2 domains. The C2 domains, which have been shown to be essential for both synaptic vesicle exocytosis and endocytosis, are also seen as the Ca2+ sensors in synaptic vesicular release. In a previous study, we reported that a polyclonal antibody raised against the squid (Loligo pealei) Syt I C2B domain, while inhibiting vesicular endocytosis, was synaptic release neutral at the squid giant synapse. Recent reports concerning the C2B requirements for synaptic release prompted us to readdress the role of C2B in squid giant synapse function. Presynaptic injection of another anti-Syt I-C2B antibody (using recombinant whole C2B domain expressed in mammalian cell culture as an antigen) into the presynaptic terminal reproduced our previous results, i.e., reduction of vesicular endocytosis without affecting synaptic release. This set of results addresses the issue of the geometrical arrangement of the Ca2+ sensor, allowing the C2B domain antibody to restrict Ca2+-dependent C2B self-oligomerization without modifying the Ca2+-dependent release process.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=539760Documentos Relacionados
- Role of the C2B domain of synaptotagmin in vesicular release and recycling as determined by specific antibody injection into the squid giant synapse preterminal.
- Role of the C2A domain of synaptotagmin in transmitter release as determined by specific antibody injection into the squid giant synapse preterminal.
- C2A activates a cryptic Ca2+-triggered membrane penetration activity within the C2B domain of synaptotagmin I
- Interaction of the synprint site of N-type Ca2+ channels with the C2B domain of synaptotagmin I
- Block of transmitter release by botulinum C1 action on syntaxin at the squid giant synapse