Aufgrund von Vorbereitungen auf eine neue Version von KOPS, können kommenden Montag und Dienstag keine Publikationen eingereicht werden. (Due to preparations for a new version of KOPS, no publications can be submitted next Monday and Tuesday.)
Type of Publication: | Journal article |
URI (citable link): | http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-81983 |
Author: | Leist, Marcel; Fava, Eugenio; Montecucco, Cesare; Nicotera, Pierluigi |
Year of publication: | 1997 |
Published in: | European Journal of Neuroscience ; 9 (1997), 7. - pp. 1488-1498. - ISSN 0953-816X. - eISSN 1460-9568 |
DOI (citable link): | https://dx.doi.org/10.1111/j.1460-9568.1997.tb01503.x |
Summary: |
Endogenous generation of nitric oxide and its congeners, including peroxynitrite (ONOO-), has been implicated in the mechanism of neuron loss in neurodegenerative diseases. Accordingly, nitric oxide donors and ONOO-can elicit both apoptosis and necrosis in neuron cultures. Here we show that nitric oxide donors and ONOO- are each able to trigger apoptosis of mouse cerebellar granule cells by an excitotoxic mechanism requiring exocytosis and NMDA receptor-mediated intracellular Ca2+ overload. This conclusion is supported by the following findings. Apoptosis was induced by various nitric oxide donors or by direct addition of ONOO- to differentiated cerebellar granule cell cultures that were sensitive to NMDA toxicity, but not in cerebellar granule cells that did not display NMDA-induced cell death (i.e. early days in culture) or in various glial cell populations. Donors of ONOO- or nitric oxide stimulated a sustained increase in intracellular Ca2+, which was prevented by inhibitors of NMDA receptors, such as MK-801 and 5-phospho-aminovaleric acid, or by dampening neuronal electrical activity with high concentrations of extracellular Mg2+. Moreover, these treatments and the exposure of cerebellar granule cells in nominally Ca2+-free media prevented apoptotic cell death. Both the intracellular Ca2+ increase and apoptosis elicited by ONOO- or the nitric oxide donors were prevented by blocking exocytosis with tetanus toxin or botulinum neurotoxin C.
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Subject (DDC): | 570 Biosciences, Biology |
Keywords: | apoptosis, mouse, clostridial neurotoxins, peroxynitrite, NMDA receptor |
Link to License: | In Copyright |
LEIST, Marcel, Eugenio FAVA, Cesare MONTECUCCO, Pierluigi NICOTERA, 1997. Peroxynitrite and Nitric Oxide Donors Induce Neuronal Apoptosis by Eliciting Autocrine Excitotoxicity. In: European Journal of Neuroscience. 9(7), pp. 1488-1498. ISSN 0953-816X. eISSN 1460-9568. Available under: doi: 10.1111/j.1460-9568.1997.tb01503.x
@article{Leist1997Perox-8264, title={Peroxynitrite and Nitric Oxide Donors Induce Neuronal Apoptosis by Eliciting Autocrine Excitotoxicity}, year={1997}, doi={10.1111/j.1460-9568.1997.tb01503.x}, number={7}, volume={9}, issn={0953-816X}, journal={European Journal of Neuroscience}, pages={1488--1498}, author={Leist, Marcel and Fava, Eugenio and Montecucco, Cesare and Nicotera, Pierluigi} }
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