US EPA

2305634 

Journal Article 

An ultrastructural study of methylmercury-induced primary sensory neuropathy in the rat 

Herman, SP; Klein, R; Talley, FA; Krigman, MR 

1973 

1 

Laboratory Investigation
ISSN: 0023-6837
EISSN: 1530-0307 

28 

1 

104-118 

English 

4569929 

WOS:A1973O847800014 

HEEP COPYRIGHT: BIOL ABS. Experimental Minamata disease was produced in 16 rats by injecting methylmercury hydroxide (MMH) s.c., 2 mg Hg/kg/day, for 1-3 wk. Ataxic hindlimb gait appeared around day 20. Light microscopic examination of the peripheral nerves, spinal ganglia and cord revelaed the evolution of a sensory polyneuropathy with selective Wallerian-like degeneration of sensory fibers in dorsal root, sciatic nerve, brachial plexus and sural nerve. Ventral roots were less affected. Coincident with collapse of sensory axons, ganglion cells displayed neuronophagia and Nageotte body formation. These changes began several days prior to the onset of ataxia and at least 1 wk prior to CNS neuronal necrosis. Ultrastructural examination of spinal ganglion cells revelaed the progressive disorganization and disappearance of rough endoplasmic reticulum, Golgi apparatuses, neurofibrils, ribosomes and polysomes. The most devastated area of the perikaryon was beneath the plasmalemma, quite unlike the perinuclear loss of organelles in central chromatolysis. Peripheral sensory axons revealed the typical ulstrastructural pattern of Wallerian degeneration. The spinal ganglion cell is the primary target of MMH in the peripheral nervous system. Only a neuropathy induced by MMH in the rat must be added to the small number of disease entities known to be associated with primary sensory neuropathy. MMH may inhibit protein synthesis within the ganglion cell perikarya as suggested by the disorganization of protein synthesizing apparatuses of the ultrastructural level.