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

Synapsin I is involved in regulating amino acid neurotransmitter release, b ut has a less clear role in noradrenergic nerve terminals. To better unders tand the role of synapsin I in the function of noradrenergic nerve terminal s, we compared noradrenaline release in wild-type and synapsin I-deficient mice. No difference was found in the accumulation or in the Ca2+-independen t release of [H-3]noradrenaline in cerebrocortical synaptosomes from wild-t ype and synapsin I-deficient mice. Synaptosomes lacking synapsin I also dis played no gross alterations in either the time course or the Ca2+-dependenc y of [H-3]noradrenaline release when stimulated by depolarizing secretagogu es or ionophore treatment. In wild-type synaptosomes, activation of protein kinase C by phorbol ester treatment resulted in a Ca2+-dependent increase in [H-3]noradrenaline release evoked by depolarizing secretagogues and iono phore treatment. The phorbol ester-mediated enhancement of [H-3]noradrenali ne release evoked by depolarizing secretagogues, but not by ionophore treat ment, was greatly reduced in synapsin I-deficient synaptosomes. These resul ts indicate that synapsin I plays a role in regulating noradrenaline releas e. (C) 2000 Wiley-Liss, Inc.