Is Calcium Accumulation Post-Injury an Indicator of Cell Damage?

Abstract

It is generally agreed that excessive intracellular calcium accumulation is the main culprit for nerve cell damage following brain injury. Many autoradiographic studies of the post-injury brain have demonstrated an accumulation of 45Ca2+ in regions exhibiting neuronal damage. We have recently observed, after cortical contusion trauma [10], that there was a discrepancy between the extent of cell damage and the extent of 45Ca2+ in autoradiograms; rather the distribution of 45Ca2+ followed that of serum proteins. In addition 45Ca2+ was also observed in white matter, which had no signs of damage. We tested the hypothesis that 45Ca2+ accumulation was coupled to the presence of protein by directly injecting albumin into the brain cortex. There was a highly significant correlation between the content of 45Ca2+ and of albumin as measured by ELISA. A similar pattern was found after a cortical freeze-lesion in the contralateral hemisphere. However, in the ipsilateral hemisphere where cell damage was observed, the relation broke down and calcium accumulated in excess. We conclude that calcium accumulation in the brain is not only the result of cell damage but also of the presence of calcium-binding proteins, e.g. albumin.