open access

Vol 51, No 4 (2013)
Original paper
Submitted: 2014-02-05
Accepted: 2014-02-05
Published online: 2014-02-05
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Relationships between calpains and glutamate- or kainate-induced apoptosis in Xenopus laevis tadpoles

Claire Brun, Elara Moudilou, Caroline Bouchot, Lucie Abrouk-Vérot, Jean-Marie Exbrayat
DOI: 10.5603/FHC.2013.0041
·
Folia Histochem Cytobiol 2013;51(4):300-311.

open access

Vol 51, No 4 (2013)
ORIGINAL PAPERS
Submitted: 2014-02-05
Accepted: 2014-02-05
Published online: 2014-02-05

Abstract

Abstract: Cell glutamate-damage induced by overstimulation of ionotropic receptors is initiated by modification of the intracellular Ca2+ homeostasis and the concomitant activation of Ca2+-dependent cysteine proteases, the calpain and caspase families. The resultant cleavage of target molecules mediates a critical function in the execution of the cell death. In this work, we investigated relationships between the activity of calpain and glutamate-orkainate-induced apoptosis in several organs of Xenopus laevis tadpole. Animals (stage 48) were incubated for 3 hours with glutamate (30–120 mM) or kainate (0.015–0.75 mM) and the rise of both apoptosis and calpain was observed in several organs. Our results indicated that glutamate (120 mM) or kainate (0.15 mM) exposure induced cell death with apoptotic features. The toxic effects of drugs into the organs were variable. Apoptosis was probably not the only form of cell death and option of necrosis or apoptosis was depending on the stimulation degree of the receptor, i.e. the receptor type, intensity and time course of molecule exposure. The increase of ubiquitous calpain was not correlated with the peak of apoptosis, suggesting the role of calpain in cell death was complex: calpain and caspase pathways were tightly interrelated in the glutamate- or kainate-induced cell death and the contribution of calpain to another type of death than apoptosis was perhaps preferred.

Abstract

Abstract: Cell glutamate-damage induced by overstimulation of ionotropic receptors is initiated by modification of the intracellular Ca2+ homeostasis and the concomitant activation of Ca2+-dependent cysteine proteases, the calpain and caspase families. The resultant cleavage of target molecules mediates a critical function in the execution of the cell death. In this work, we investigated relationships between the activity of calpain and glutamate-orkainate-induced apoptosis in several organs of Xenopus laevis tadpole. Animals (stage 48) were incubated for 3 hours with glutamate (30–120 mM) or kainate (0.015–0.75 mM) and the rise of both apoptosis and calpain was observed in several organs. Our results indicated that glutamate (120 mM) or kainate (0.15 mM) exposure induced cell death with apoptotic features. The toxic effects of drugs into the organs were variable. Apoptosis was probably not the only form of cell death and option of necrosis or apoptosis was depending on the stimulation degree of the receptor, i.e. the receptor type, intensity and time course of molecule exposure. The increase of ubiquitous calpain was not correlated with the peak of apoptosis, suggesting the role of calpain in cell death was complex: calpain and caspase pathways were tightly interrelated in the glutamate- or kainate-induced cell death and the contribution of calpain to another type of death than apoptosis was perhaps preferred.
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Keywords

calpain; apoptosis; ecotoxicity; glutamate receptors; calcium; Xenopus laevis

About this article
Title

Relationships between calpains and glutamate- or kainate-induced apoptosis in Xenopus laevis tadpoles

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 51, No 4 (2013)

Article type

Original paper

Pages

300-311

Published online

2014-02-05

DOI

10.5603/FHC.2013.0041

Bibliographic record

Folia Histochem Cytobiol 2013;51(4):300-311.

Keywords

calpain
apoptosis
ecotoxicity
glutamate receptors
calcium
Xenopus laevis

Authors

Claire Brun
Elara Moudilou
Caroline Bouchot
Lucie Abrouk-Vérot
Jean-Marie Exbrayat

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