Sensitivity to 4-aminopyridine observed in mammalian sciatic nerves during acute pyridoxine-induced sensory neuropathy and recovery
In vitro physiologic properties of rat sciatic nerve were examined during pyridoxine-induced sensory neuropathy and following recovery. Compound action potential waveform characteristics, recovery cycle properties during paired stimulation, and ability to follow stimuli presented at high frequencies...
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Published in | Experimental neurology Vol. 100; no. 3; pp. 448 - 458 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier Inc
01.06.1988
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | In vitro physiologic properties of rat sciatic nerve were examined during pyridoxine-induced sensory neuropathy and following recovery. Compound action potential waveform characteristics, recovery cycle properties during paired stimulation, and ability to follow stimuli presented at high frequencies were examined. All parameters were assessed before and after potassium channel blockade with 4-aminopyridine in nerves from acutely toxic, recovered, and age-matched control rats. Compound action potential waveforms recorded from acutely toxic nerves were less affected by application of 4-aminopyridine than were those recorded from control nerves. Recovery cycles were less prolonged and frequency-following abilities less compromised following the drug in these experimental nerves than in controls. In contrast, after a 3-month recovery period, experimental nerves demonstrated a more pronounced sensitivity to 4-aminopyridine than did age-matched control nerves. It is proposed that these differences in the physiological effects of 4-aminopyridine reflect the selective loss of large-caliber sensory fibers during the acute toxic phase and the increased sensitivity to the drug of regenerated sensory fibers following recovery. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0014-4886 1090-2430 |
DOI: | 10.1016/0014-4886(88)90030-1 |