Ultrastructural dystrophic changes in central sensory synaptic terminals in clarke's nucleus neuropil after neonatal seiatic nerve crush

ABSTRACT

The present investigation demonstrates the long-term dystrophic changes in primary sensory terminals within Clarke's nucleus of young adult rats [12 weeks of age] whose sciatic nerves were subjected to crush injury at birth. Variable degrees of dystrophic changes were observed in the affected axon terminals. These changes included hyperplasia of neurofilaments, accumulation of electron-dense bodies, clustering of synaptic vesieles, distortion of mitochondria, collections of vesicular profiles and vacuoles and engulfment of some terminals by reactive glial cell processes. Accumulation of dense bodies and replacement of synaptic vesieles by neurofilaments were the most frequent features. In the control specimens of the same animals, dystrophie changes were rarely observed. These dystrophie changes are most probably due to transganglionic atrophy caused by defective axonal transport mechanisms from their hypoplastic perikarya in the dorsal root ganglia. Coupled with future studies on the axonal metabolism, these ultrastructural observations will contribute to the understanding of the alterations in the spinal cord synaptic transmission and of the abnormal sensory symptoms associated with peripheral nerve lesions