ELECTROPHYSIOLOGY OF METHYL MERCURY POISONING

¹ Department of Physiology and Pharmacology, Duke University, Durham, North Carolina; The National institute of Environmental Health Sciences, Research Triengle Park, North Carolina

Rats were treated by s.c. injections of methyl mercury hydroxide (MeHg⁺) for three to four weeks until they developed ataxia and abnormal reflexes of the hindlegs. In these animals the compound action potential evoked in dorsal roots by stimulation of the sciatic nerve showed retardation of the conduction velocity, elevation of the (extracellular) threshold and, most conspicuously, a reduction of amplitude and "area." The compound action potential of ventral roots was only minimally affected. Upon intracellular stimulation of individual spinal ganglion cells, there was evidence neither of elevation of the rheobase, nor of a change of resting membrane potential or of membrane resistance. The intracellularly recorded spike potential of many poisoned sensory ganglion cells was strikingly prolonged, and these abnormal spikes showed a "plateau" or "shoulder" indicating retarded repolarization. There was evidence of minor weakening of skeletal muscle when stimulated through its motor nerve, which could have been caused by the loss of a small number of motor units, and consequent scattered focal denervation atrophy. It is concluded from these observations, and from other publications, that MeHg⁺ poisoning affects sensory ganglion cell bodies first, with secondary degeneration of sensory axons. Neurons with axons of large caliber appeared to be lost in larger numbers than smaller ones. Clinical electroneurography may be a valuable tool for following the course of poisoning by alkyl mercurials after diagnosis is firmly establisimed, but not for early detection of suspected cases.