| Kainic acid-induced neuronal cell death in cerebellar granule cells is not prevented by caspase inhibitors. | |
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MedLine Citation:
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PMID: 11877339 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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1. We examined the role of non-NMDA receptors in kainic acid (KA)-induced apoptosis in cultures of rat cerebellar granule cells (CGCs). KA (1 - 500 microM) induced cell death in a concentration-dependent manner, which was prevented by NBQX and GYKI 52466, non-NMDA receptor antagonists. Moreover, AMPA blocked KA-induced excitotoxicity, through desensitization of AMPA receptors. 2. Similarly, KA raised the intracellular calcium concentration of CGCs, which was inhibited by NBQX and GYKI 52466. Again, AMPA (100 microM) abolished the KA (100 microM)-induced increase in intracellular calcium concentration. 3. KA-induced cell death in CGCs had apoptotic features, which were determined morphologically, by DNA fragmentation, and by expression of the prostate apoptosis response-4 protein (Par-4). 5. KA (500 microM) slightly (18%) increased caspase-3 activity, which was strongly enhanced by colchicine (1 microM), an apoptotic stimulus. However, neither Z-VAD.fmk, a pan-caspase inhibitor, nor the more specific caspase-3 inhibitor, Ac-DEVD-CHO, prevented KA-induced cell death or apoptosis. In contrast, both drugs inhibited colchicine-induced apoptosis. 5. The calpain inhibitor ALLN had no effect on KA or colchicine-induced neurotoxicity. 6. Our findings indicate that colchicine-induced apoptosis in CGCs is mediated by caspase-3 activation, unlike KA-induced apoptosis. |
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Authors:
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Ester Verdaguer; Elvira García-Jordà; Andrés Jiménez; Alessandra Stranges; Francesc X Sureda; Anna M Canudas; Elena Escubedo; Jordi Camarasa; Mercè Pallàs; Antoni Camins |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: British journal of pharmacology Volume: 135 ISSN: 0007-1188 ISO Abbreviation: Br. J. Pharmacol. Publication Date: 2002 Mar |
Date Detail:
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Created Date: 2002-03-05 Completed Date: 2002-08-16 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7502536 Medline TA: Br J Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 1297-307 Citation Subset: IM |
Affiliation:
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Unitat de Farmacologia i Farmacognòsia, Facultat de Farmàcia, Universitat de Barcelona, Nucli Universitari de Pedralbes, E-08028 Barcelona, Spain. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects* Apoptosis Regulatory Proteins Carrier Proteins / metabolism Caspase 3 Caspases / antagonists & inhibitors* Cell Survival / drug effects Cells, Cultured Cerebellum / cytology, drug effects*, metabolism Cysteine Proteinase Inhibitors / pharmacology Enzyme Precursors / antagonists & inhibitors Intracellular Signaling Peptides and Proteins* Kainic Acid / toxicity* Neurons / drug effects*, metabolism Rats Rats, Sprague-Dawley Receptors, AMPA / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Apoptosis Regulatory Proteins; 0/Carrier Proteins; 0/Cysteine Proteinase Inhibitors; 0/Enzyme Precursors; 0/Intracellular Signaling Peptides and Proteins; 0/Receptors, AMPA; 0/prostate apoptosis response-4 protein; 487-79-6/Kainic Acid; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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