Calpain Activity in Spinal Cord Cells from Rats with Experimental Allergic Encephalomyelitis of Different Grades

Abstract

The Ca2+-dependent calpain system of intracellular proteases is involved in regulating a multitude of physiological body functions. However, hyperactivation of calpains in cells is observed during the development of a number of responses, and this leads to impairment to the functioning of vitally important physiological systems. We report here our use of a model of experimental allergic encephalomyelitis (EAE) to demonstrate that cell homogenates from different parts of spinal cord show hyperactivation of calpains and that calpain proteolytic activity increases with the severity of EAE; this occurred not only in the lower, but also in the upper parts of the spinal cord. As CNS cells from animals with EAE showed increases in the levels of mRNA for m- but not for μ-calpain, this hyperactivation would appear to be mediated more by m-calpain. The relationship between the distribution of m-calpain hyperactivation in different parts of the spinal cord with the severity of EAE is consistent with data on the volume of neurological destruction of the CNS, suggesting that m-calpain is involved in the processes initiating neuron and cell death during the development of this disease.