Abstract
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 Ca2+-independent release of [3H]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 Ca2+-dependency of [3H]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 Ca2+-dependent increase in [3H]noradrenaline release evoked by depolarizing secretagogues and ionophore treatment. The phorbol ester-mediated enhancement of [3H]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.
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