In:
Journal of Neurochemistry, Wiley, Vol. 52, No. 2 ( 1989-02), p. 370-376
Kurzfassung:
Abstract: Botulinum C2 toxin is known to ADP‐ribosylate actin. The toxin effect was studied on [ 3 H]noradrenaline secretion of PC12 cells. [ 3 H]Noradrenaline release was stimulated five‐ to 15‐fold by carbachol (100 μ M ) or K + (50 m M ) and 10–30‐fold by the ionophore A23187 (5 μ M ). Pretreatment of PC12 cells with botulinum C2 toxin for 4–8 h at 20°C, increased carbachol‐, K + ‐, and A23187‐induced, but not basal, [ 3 H]noradrenaline release maximally 1.5‐ to threefold, whereas ≥75% of the cellular actin pool was ADP‐ribosylated. Treatment of PC12 cells with botulinum C2 toxin for up to 1 h at 37°C also increased stimulated [ 3 H]noradrenaline secretion, whereas toxin treatment for 〉 1 h decreased the enhanced [ 3 H]noradrenaline release stimulated by carbachol and K + but not by A23187. Concomitantly with toxin‐induced stimulation of secretion, 20–50% of the cellular actin was ADP‐ribosylated, whereas 〉 60% of actin was modified when exocytosis was attenuated. The data indicate that ADP‐ribosylation of actin by botulinum C2 toxin largely modulates stimulation of [ 3 H]noradrenaline release. Moreover, the biphasic toxin effects suggest that distinct mechanisms are involved in the role of actin in secretion.
Materialart:
Online-Ressource
ISSN:
0022-3042
,
1471-4159
DOI:
10.1111/jnc.1989.52.issue-2
DOI:
10.1111/j.1471-4159.1989.tb09131.x
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
1989
ZDB Id:
2020528-4
SSG:
12
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