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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Decrease in phorbol ester-induced potentiation of noradrenaline release in synapsin I-deficient mice.

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.[1]

References

  1. Decrease in phorbol ester-induced potentiation of noradrenaline release in synapsin I-deficient mice. Walaas, S.I., Hilfiker, S., Li, L., Chin, L.S., Greengard, P. Synapse (2000) [Pubmed]
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