Cell glutamate-damage induced by overstimulation of ionotropic receptors is initiated by modification of the intracellular Ca 2+ homeostasis and the concomitant activation of Ca 2+ -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-or kainate-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.