Zusammenfassung
Sehr wahrscheinlich spielt Adenosin in verschiedenen Geweben einschließlich des Zentralnervensystems eine Rolle als autokriner/parakriner Regulator. Dies ist in Abb. 1 schematisch dargestellt. Adenosinspiegel im Gewebe steigen nach Hypoxie und/oder Ischämie an, ebenso nach langfristiger Aktivierung eines Nervs. Adenosin stammt entweder aus den Nervenzellen selbst oder wird während der Aktivität des Nervs von Effektorzellen abgegeben. Es wurde wiederholt festgestellt, daß es eher post- als präsynaptisch produziert wird [la, 2]. Es wird nicht aus Speichern abgerufen, sondern bei Bedarf freigesetzt. Eine mögliche Quelle ist das von Nerven- oder Effektorzellen während der Transmission ausgeschüttete ATP. Dies wurde wiederholt von Burnstock [1] postuliert, und es dürften kaum Zweifel daran bestehen, daß ATP zumindest in der Peripherie als wichtiger Botenstoff an der Neurotransmission beteiligt ist.
Ich danke Dres’. Marianne Dunér-Engström, Ping-Sheng Hu, Ingeborg van der Ploeg, Johan Fastbom, Thomas Dunwiddie, Fiona Parkinson, Herrn Sten Ågren sowie Frau Agneta Wallman für ihre Unterstützung. Die Untersuchungen wurden durch Forschungsbeihilfen der Loo and Hans Ostermans Foundation, der 1987 Foundation for Stroke Research des Swedish Medical Research Council, des Karolinksa Institut unterstützt.
Übersetzung: Birgit Lamerz-Beckschäfer.
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© 1992 Springer-Verlag Berlin Heidelberg
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Fredholm, B.B. (1992). Wirkmechanismus von Adenosin und Vinpocetin. In: Lungershausen, E. (eds) Demenz. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76932-0_13
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