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Decrease in phorbol ester‐induced potentiation of noradrenaline release in synapsin I‐deficient mice
Author(s) -
Walaas S. Ivar,
Hilfiker Sabine,
Li Lian,
Chin LihShen,
Greengard Paul
Publication year - 2000
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(200005)36:2<114::aid-syn4>3.0.co;2-q
Subject(s) - synapsin , long term potentiation , synapsin i , phorbol ester , chemistry , phorbol , pharmacology , microbiology and biotechnology , biochemistry , biology , signal transduction , protein kinase c , receptor , synaptic vesicle , vesicle , membrane
Synapsin I is involved in regulating amino acid neurotransmitter release, but has a less clear role in noradrenergic nerve terminals. To better understand the role of synapsin I in the function of noradrenergic nerve terminals, we compared noradrenaline release in wild‐type and synapsin I‐deficient mice. No difference was found in the accumulation or in the Ca 2+ ‐independent release of [ 3 H]noradrenaline in cerebrocortical synaptosomes from wild‐type and synapsin I‐deficient mice. Synaptosomes lacking synapsin I also displayed no gross alterations in either the time course or the Ca 2+ ‐dependency of [ 3 H]noradrenaline release when stimulated by depolarizing secretagogues or ionophore treatment. In wild‐type synaptosomes, activation of protein kinase C by phorbol ester treatment resulted in a Ca 2+ ‐dependent increase in [ 3 H]noradrenaline release evoked by depolarizing secretagogues and ionophore treatment. The phorbol ester‐mediated enhancement of [ 3 H]noradrenaline release evoked by depolarizing secretagogues, but not by ionophore treatment, was greatly reduced in synapsin I‐deficient synaptosomes. These results indicate that synapsin I plays a role in regulating noradrenaline release. Synapse 36:114–119, 2000. © 2000 Wiley‐Liss, Inc.