Changes in the distribution of fast and slow forms of troponin I in some neuromuscular disorders.

As judged from the atrophy of the muscle cells, the distribution of slow and fast troponin I in type I and type II cells in peripheral neuropathies in the adults (24-67 years of age) was unaffected for long periods after denervation. Reinnervation by fast or slow nerve in chronic neuropathies usually resulted in typical fibre type grouping with complete segregation of slow and fast troponin I in type I and type II cells, respectively. Intermediate fibres (slow and fast troponin I in the same cell) were present during the course of transformation. Unlike peripheral neuropathies, the number of cells staining for slow troponin I in the very atrophic fascicles in spinal muscular atrophy was considerably reduced. The synthesis of fast troponin I was stimulated in original type I cells containing slow troponin I. These observations support the experimental data (Dhoot and Perry 1982b) that the suppression of fast troponin I in type I or presumptive type I cells requires innervation by the slow nerve. Its absence results in an increased expression of fast troponin I in cells that originally contained only slow troponin I. Once suppressed, fast troponin I is absent in type I cells even after long periods of experimental denervation or cases of human peripheral neuropathies but not so in the cases of spinal muscular atrophy.