The evolution of intracellular responses to acrylamide in rat spinal ganglion neurons

Acrylamide (30 mg or 50 mg/kg/day, 5 days each week) was injected intraperitoneally into rats for up to 4 weeks. Lumbar spinal ganglia, spinal cord and lumbrical muscle spindles were examined by light and electron microscopy at various times during this period. The first abnormalities in spinal ganglion neurons were seen at 7 days when an apparent increase in numbers of mitochondria, some being hypertrophic, were found in a few large light cells. This was 10 days before any significant Wallerian degeneration was found in muscle spindle sensory fibres. Mitochondrial changes became more marked with time and were later associated with RER disruption, loss of neurofilaments and peripheral displacement of the nucleus thus mimicking chromatolysis of the axon reaction. All these changes began, however, before axon degeneration. Evidence of increased satellite cell activity was maximal at 21 days. These changes are discussed in the light of the possibility that calcium entry into the cell may be seriously increased early in the intoxication as a direct result of the presence of acrylamide and that many of these cellular features are secondary responses to such an event. Distal degeneration of axons seems likely to be secondary to the perikaryal changes.