[Calcium transport mechanisms in neuroprotection and neurotoxicity]

Calcium (Ca²(+)) has been found to be involved in neuroprotective processes, by triggering enzymatic cascades that are essential for the synthesis and functioning of the elements that carry out this process. However, it is paradoxical that this ion is one of the main initiators of apoptotic cascades. This difference in its effects is conditioned by differences in the cytoplasmic concentrations.

Ca²(+) plays a role in the activation of antiapoptotic signals in the neuron when its levels rise moderately, but it also starts apoptotic processes that are triggered mainly by its accumulation in mitochondria. This Ca²(+) comes from the outside or from intracellular deposits by means of different types of transporters. In order to assess the role of Ca²(+) in these processes, it is necessary to consider all the means of transport in an integral manner, since manipulating it pharmacologically gives rise to either protective or toxic processes, due to alterations in the intracellular concentrations of the ion.

Notable progress has been made in the understanding of the effects of Ca²(+) on the central nervous system and on the mechanisms for controlling and transporting it. It is important to stress that understanding these physiological processes has led to the development of drugs with protective effects and, although most of them are still in the study phase or display important side effects, it remains a promising field that will help in the development of useful therapeutic strategies in neuroprotection.