Studies on drug-induced neuropathies. III. Motor nerve deficit in cats with experimental acrylamide neuropathy

• Published in: European journal of pharmacology Vol. 35; no. 1; p. 177
• Main Authors: Lowndes, H E, Baker, T
• Format: Journal Article
• Language: English
• Published: Netherlands 01-01-1976
• Subjects: Acrylamides - pharmacology; Animals; Cats; Electric Stimulation; Male; Motor Neurons - drug effects; Muscle Contraction - drug effects; Muscles - physiology; Nerve Endings - drug effects; Nervous System Diseases - chemically induced; Neural Conduction - drug effects; Time Factors
• ISSN: 0014-2999
• DOI: 10.1016/0014-2999(76)90313-7

To assess motor nerve and motor nerve terminal function in acrylamide neuropathy, cats were given i.m. injections of acrylamide (15 mg/kg) daily for 10 days to induce a peripheral neuropathy. Tests of function were performed on the day of the 10th injection (day 0) and 7, 21 and 35 days thereafter. In untreated animals tetanic conditioning evoked stimulus-bound repetition (SBR) in 85% of soleus alpha-motoneurones. Following administration of acrylamide, the percent of axons elaborating SBR were: day 0 -- 79%, day 7 -- 71%, day 21 -- 31%, day 35 -- 22%. The response of soleus muscle to SBR is normally a post-tetanic potentiation (PTP) of contractile tension which is proportional to the tetanic conditioning frequency; during the development of the neuropathy, PTP in response to all tetanic frequencies progressively declined, concomitant with and as a result of the declining incidence of SBR. These data indicate that initial functional alterations in motor nerves during acrylamide neuropathy occurs at the level of the nerve terminal, preceding alterations in conduction velocities in the axons. However, the motor nerve deficit is not adequate, in either time to onset or severity, to account for the clinical manifestations of the neuropathy. The possible contribution to clinical signs of the neuropathy made by lesions to other peripheral nerves is discussed.