2003
DOI: 10.1016/s0006-8993(02)04080-5
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Colchicine induces apoptosis in organotypic hippocampal slice cultures

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Cited by 70 publications
(47 citation statements)
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“…34 When colchicin, being a strong microtubule-depolymerizing agent, is implemented intracranially in experimental studies, it causes deficits in memory 35 which is thought to be related by inducing apoptosis. 36 Therefore, it is used as a selective neurotoxin in the animal models for Alzheimer disease and epilepsy. 35 However, in its usage in humans, it is reported that its absorption is rapid in oral use and presenting in high concentrations in kidney, liver and spleen whereas it is not absorbed by heart, skeletal muscle and brain.…”
Section: Discussionmentioning
confidence: 99%
“…34 When colchicin, being a strong microtubule-depolymerizing agent, is implemented intracranially in experimental studies, it causes deficits in memory 35 which is thought to be related by inducing apoptosis. 36 Therefore, it is used as a selective neurotoxin in the animal models for Alzheimer disease and epilepsy. 35 However, in its usage in humans, it is reported that its absorption is rapid in oral use and presenting in high concentrations in kidney, liver and spleen whereas it is not absorbed by heart, skeletal muscle and brain.…”
Section: Discussionmentioning
confidence: 99%
“…As a control, we assessed Ac-DEVD-AMC cleavage following treatment with colchicine (10 M). Colchicine inhibits microtubule polymerization and has been shown to induce apoptosis in cerebral granular neurons (5) and organotypic slices (33). We observed no significant difference in caspase 3-like protease activities between WT and puma Ϫ/Ϫ neuron cultures following colchicine treatment (Fig.…”
Section: Resultsmentioning
confidence: 58%
“…This study also offers the first indication that the self-aggregation CaMKIIα is dependent on microtubule stability, and it introduces p600 as the mediator of this effect. Since Ca 2+ overload, microtubule instability and p600 depletion have all been independently shown to cause neuronal death [17,34,35], this study puts us closer to a unified model wherein p600 is an interface between microtubule dynamics, Ca 2+ signalling, and neuronal survival.…”
Section: Discussionmentioning
confidence: 79%