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Calpain activation in okadaic-acid-induced neurodegeneration.
Neuroreport 2006; 17(7):689-92N

Abstract

Calpain activation has been implicated in the pathogenesis of Alzheimer's disease. Okadaic acid, a protein phosphatase-2A inhibitor, has been used in Alzheimer's disease research models to increase tau phosphorylation and induce neuronal death. We previously reported that okadaic acid induced predominant activation of caspase-3 in immature neurons, but less activation in mature neurons. We found here that, in okadaic-acid-treated mature neurons, levels of an inactive form of m-calpain decreased and levels of calpain-cleaved spectrin and synapsin-I fragments increased, suggestive of calpain activation. Pretreatment with calpain inhibitor decreased lactate dehydrogenase release by 20% and increased average dendritic branch length by 50% compared with neurons treated with okadaic acid alone. These findings suggest that calpain is activated during okadaic-acid-induced neurodegeneration and calpain inhibition can be protective against it.

Authors+Show Affiliations

Department of Anatomy and Cell Biology, University of Ulsan College of Medicine, Seoul, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16641670

Citation

Yoon, SeungYong, et al. "Calpain Activation in Okadaic-acid-induced Neurodegeneration." Neuroreport, vol. 17, no. 7, 2006, pp. 689-92.
Yoon S, Choi J, Huh JW, et al. Calpain activation in okadaic-acid-induced neurodegeneration. Neuroreport. 2006;17(7):689-92.
Yoon, S., Choi, J., Huh, J. W., Hwang, O., & Kim, D. (2006). Calpain activation in okadaic-acid-induced neurodegeneration. Neuroreport, 17(7), pp. 689-92.
Yoon S, et al. Calpain Activation in Okadaic-acid-induced Neurodegeneration. Neuroreport. 2006 May 15;17(7):689-92. PubMed PMID: 16641670.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calpain activation in okadaic-acid-induced neurodegeneration. AU - Yoon,SeungYong, AU - Choi,JungEun, AU - Huh,Jae-Wan, AU - Hwang,Onyou, AU - Kim,DongHou, PY - 2006/4/28/pubmed PY - 2006/7/27/medline PY - 2006/4/28/entrez SP - 689 EP - 92 JF - Neuroreport JO - Neuroreport VL - 17 IS - 7 N2 - Calpain activation has been implicated in the pathogenesis of Alzheimer's disease. Okadaic acid, a protein phosphatase-2A inhibitor, has been used in Alzheimer's disease research models to increase tau phosphorylation and induce neuronal death. We previously reported that okadaic acid induced predominant activation of caspase-3 in immature neurons, but less activation in mature neurons. We found here that, in okadaic-acid-treated mature neurons, levels of an inactive form of m-calpain decreased and levels of calpain-cleaved spectrin and synapsin-I fragments increased, suggestive of calpain activation. Pretreatment with calpain inhibitor decreased lactate dehydrogenase release by 20% and increased average dendritic branch length by 50% compared with neurons treated with okadaic acid alone. These findings suggest that calpain is activated during okadaic-acid-induced neurodegeneration and calpain inhibition can be protective against it. SN - 0959-4965 UR - https://www.unboundmedicine.com/medline/citation/16641670/Calpain_activation_in_okadaic_acid_induced_neurodegeneration_ L2 - http://Insights.ovid.com/pubmed?pmid=16641670 DB - PRIME DP - Unbound Medicine ER -