Calpain inhibitors prevent nitric oxide-triggered excitotoxic apoptosis

The pathogenesis of some neurodegenerative disorders has been linked to excitotoxicity, excess generation of nitric oxide (NO) and apoptosis. Here, we used a model of NO-triggered neuronal apoptosis that was strictly dependent on autocrine NMDA receptor (NMDA-R) activation and intracellular Ca incre...

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Veröffentlicht in:	Neuroreport 2001-12, Vol.12 (17), p.3645-3648
Hauptverfasser:	Volbracht, Christiane, Fava, Eugenio, Leist, Marcel, Nicotera, Pierluigi
Format:	Artikel
Sprache:	eng
Schlagworte:	Ageing, cell death Animals Apoptosis - drug effects Apoptosis - physiology Autocrine Communication - drug effects Autocrine Communication - physiology Biological and medical sciences Calcium - metabolism Calcium Signaling - drug effects Calcium Signaling - physiology Calpain - antagonists & inhibitors Calpain - metabolism Carrier Proteins - metabolism Cell physiology Cells, Cultured DNA Damage - drug effects DNA Damage - physiology Dose-Response Relationship, Drug Enzyme Inhibitors - pharmacology Excitatory Amino Acid Antagonists - pharmacology Fundamental and applied biological sciences. Psychology Mice Mice, Inbred Strains Microfilament Proteins - metabolism Mitochondria - drug effects Mitochondria - metabolism Mitochondria - pathology Molecular and cellular biology Neurodegenerative Diseases - drug therapy Neurodegenerative Diseases - metabolism Neurodegenerative Diseases - physiopathology Neurons - drug effects Neurons - metabolism Neurotoxins - pharmacology Nitric Oxide - antagonists & inhibitors Nitric Oxide - metabolism Nitric Oxide Donors - pharmacology Receptors, N-Methyl-D-Aspartate - drug effects Receptors, N-Methyl-D-Aspartate - metabolism
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