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Regulatory roles of complexins in neurotransmitter release from mature presynaptic nerve terminals
Author(s) -
Ono Shoichiro,
Baux Gérard,
Sekiguchi Mariko,
Fossier Philippe,
Morel Nicolas F.,
Nihonmatsu Itsuko,
Hirata Kanako,
Awaji Takeo,
Takahashi Seiichi,
Takahashi Masami
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00225.x
Subject(s) - neurotransmitter , synaptotagmin 1 , neurotransmission , synaptic vesicle , synaptotagmin i , active zone , synapsin , biology , neuroscience , synaptic fatigue , microbiology and biotechnology , neurotransmitter agents , neural facilitation , synapse , inhibitory postsynaptic potential , receptor , central nervous system , excitatory postsynaptic potential , vesicle , biochemistry , membrane
Complexins are presynaptic proteins whose functional roles in synaptic transmission are still unclear. In cultured rat hippocampal neurons, complexins are distributed throughout the cell bodies, dendrites and axons, whereas synaptotagmin I and synaptobrevin/VAMP‐2, essential proteins for neurotransmitter release, accumulated in the synaptic‐releasing sites as early as 1 week in culture. With a maturation of synapses in vitro , complexins also accumulated in the synaptic release sites and co‐localized with synaptotagmin I and synaptobrevin/VAMP‐2 after 3–4 weeks in culture. Complexins I and II were expressed in more than 90 and 70% of the cultured neurons, respectively; however, they were largely distributed in different populations of synaptic terminals. In the developing rat brain, complexins were distributed in neuronal cell bodies in the early stage of postnatal development, but gradually accumulated in the synapse‐enriched regions with development. In mature presynaptic neurons of Aplysia buccal ganglia, injection of anticomplexin II antibody caused a stimulation of neurotransmitter release. Injection of recombinant complexin II and αSNAP caused depression and facilitation of neurotransmitter release from nerve terminals, respectively. The effect of complexin was reversed by a subsequent injection of recombinant αSNAP, and vice versa. These results suggest that complexins are not essential but have some regulatory roles in neurotransmitter release from presynaptic terminals of mature neurons.