3.8 Article

Long-term acrylamide intoxication induces atrophy of dorsal root ganglion A-cells and of myelinated sensory axons

Journal

JOURNAL OF NEUROCYTOLOGY
Volume 31, Issue 1, Pages 79-87

Publisher

KLUWER ACADEMIC PUBL
DOI: 10.1023/A:1022579817020

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We have examined the effects of acrylamide on primary sensory nerve cell bodies and their myelinated axons in chronic acrylamide intoxication. The numbers and sizes of dorsal root ganglion cell bodies (L5) and myelinated nerve fibers were estimated with sterelogical techniques in severely disabled rats which had been treated with 33.3 mg/kg acrylamide twice a week for 7.5 weeks. There was no loss of dorsal root ganglion cells or myelinated nerve fibers in the roots, the sciatic nerve, sural nerve, and a tibial nerve branch. The mean perikaryal volume of A-cells was reduced by 20% (2P < 0.001) from 50000 μm(3) in controls (CV = 0.13) to 40000 μm(3) (0.12). whereas B-cell volume was unchanged. All size-frequency distribution curves of myelinated axon area of peripheral nerves and sensory roots were shifted to the left towards smaller values in rats exposed to acrylamide. In the L5 sensory root 3 mm from the ganglion, there was a significant reduction of mean cross sectional area of myelinated axons by 14% (2 P < 0.05) from 7.6 mum(2) (0.11) in controls to 6.5 mum(2) (0.13) in intoxicated rats. The mean cross sectional area of myelinated sural nerve axons was reduced by 22% (2P < 0.001) from 8.6 μm(2) (0.08) in controls to 6.7 μm(2) (0.17) in intoxicated rats. We conclude that chronic intoxication with acrylamide leads to selective atrophy of type A dorsal root ganglion cell bodies and simultaneous atrophy along their peripheral axons, whereas neuronal B-cell bodies and motor axons are spared. It is suggested that the neuronal atrophy might well represent a defect of neurofilament synthesis and transport.

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