The involvement of the protein kinase C substrate, B-50 (GAP-43), in the release of glutamate from small clear-cored vesicles in streptolysin-O-permeated synaptosomes was studied by using anti-B-50 antibodies. Glutamate release was induced from endogenous as well as 3H-labelled pools in a [Ca2+]-dependent manner. This Ca2+-induced release was partially ATP dependent and blocked by the light-chain fragment of tetanus toxin, demonstrating its vesicular nature. Comparison of the effects of anti-B-50 antibodies on glutamate and noradrenaline release from permeated synaptosomes revealed two major differences. Firstly, Ca2+-induced glutamate release was decreased only partially by anti-B-50 antibodies, whereas Ca2+-induced noradrenaline release was inhibited almost completely. Secondly, anti-B-50 antibodies significantly reduced basal glutamate release, but did not affect basal noradrenaline release. In view of the differences in exocytotic mechanisms of small clear-cored vesicles and large dense-cored vesicles, these data indicate that B-50 is important in the regulation of exocytosis of both types of neurotransmitters, probably at stages of vesicle recycling and/or vesicle recruitment, rather than in the Ca2+-induced fusion step. Copyright (C) 1998 Elsevier Science B.V.

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doi.org/10.1016/S0014-2999(98)00835-8, hdl.handle.net/1765/70360
European Journal of Pharmacology
Department of Internal Medicine

Hens, N, Ghijsen, W.E.J.M, Weller, U, Spierenburg, H.A, Boomsma, F, Oestreicher, A.B, … de Graan, P.N.E. (1998). Anti-B-50 (GAP-43) antibodies decrease exocytosis of glutamate in permeated synaptosomes. European Journal of Pharmacology, 363(2-3), 229–240. doi:10.1016/S0014-2999(98)00835-8