One general signalling mechanism used to transfer the information deli
vered by agonists into appropriate intracellular compartments involves
the rapid redistribution of ionised calcium throughout the cell, whic
h results in transient elevations of the cytosolic free Ca2+ concentra
tion. Various physiological stimuli increase [Ca2+], transiently and,
thereby, induce cellular responses. However, under pathological condit
ions, changes of [Ca2+], are generally more pronounced and sustained.
Marked elevations of [Ca2+], activate hydrolytic enzymes, lead to exag
gerated energy expenditure, impair energy production, initiate cytoske
letal degradation, and ultimately result in cell death. Such Ca2+-indu
ced cytotoxicity may play a major role in several diseases, including
neuropathological conditions such as chronic neurodegenerative disease
s and acute neuronal losses (e.g. in stroke).