CARBON-DISULFIDE NEUROTOXICITY IN RATS - VI - ELECTROPHYSIOLOGICAL EXAMINATION OF CAUDAL TAIL NERVE COMPOUND ACTION-POTENTIALS AND NERVE-CONDUCTION VELOCITY

The effects of subchronic exposure to carbon disulfide (CS2) on ventra l caudal tail nerve compound nerve action potential (CNAP) amplitudes and latencies, and nerve conduction velocity (NCV) in rats were examin ed. Male and female Fischer 344 rats were exposed to 0, 50, 500, or 80 0 ppm CS2 for 6 hrs/day, 5 days/week. Using separate groups, exposure duration was 2, 4, 8, or 13 weeks. Exposure to 500 or 800 ppm CS2 for 13 weeks decreased NCV compared to the 50 ppm CS2 group. CNAP amplitud es were increased, and peak P1P2 interpeak latency decreased, after ex posure to 500 or 800 ppm CS2 for 13 weeks. Most of the changes in NCV and CNAPs were not attributable to differences in tail or colonic temp erature. However, the increases in peak P-1 amplitude may relate to th e proximity of the electrodes to the rail nerves. Assessment of tail n erve morphology after 13 weeks exposure to 800 ppm CS2 revealed only m inor changes compared to the extent of axonal swelling and degeneratio n observed in the muscular branch of the tibial nerve and axonal swell ing in the spinal cord. As anticipated, in older animals the NCV incre ased, the CNAP amplitudes increased, and the CNAP latencies decreased. The biological basis for the changes in CNAPs produced by CS2 is unde r investigation. Future studies will focus on electrophysiological eva luation of spinal nerve function, to allow better correlation with pat hological and behavioral endpoints. (C) 1998 Intox Press, Inc.