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Neurotoxin-induced hydrolase activity in peripheral nerve
Neuroscience Letters
|July 17, 1981
Summary
Neurotoxins blocking axonal transport, like batrachotoxin and colchicine, significantly increased sciatic nerve hydrolase activity for weeks. This suggests nerve damage may cause prolonged enzyme elevation.
Area of Science:
- Neuroscience
- Biochemistry
- Toxicology
Background:
- Sciatic nerve hydrolase activity is crucial for nerve function.
- Neurotoxins can disrupt axonal transport and nerve impulse transmission.
- Understanding the impact of neurotoxins on nerve enzymes is vital.
Purpose of the Study:
- To investigate the effects of neurotoxins on sciatic nerve hydrolase activity.
- To differentiate the impact of axonal transport blockade versus impulse transmission blockade.
- To determine the duration of enzyme activity changes.
Main Methods:
- Subepineural injections of batrachotoxin (BTX), colchicine, and tetrodotoxin (TTX) into the sciatic nerve.
- Assay of acid protease, N-acetylglucosaminidase, and acid phosphatase activity.
- Monitoring enzyme activity over a period of up to 48 days.
Main Results:
- BTX and colchicine caused a 4-9 fold increase in acid protease and N-acetylglucosaminidase activity, lasting up to 48 days.
- Acid phosphatase activity showed a smaller increase with BTX and colchicine.
- TTX resulted in a small, transient increase in enzyme activity, returning to normal within two days.
Conclusions:
- Prolonged elevation of hydrolase activity by BTX and colchicine suggests axonal transport blockade may involve nerve necrosis.
- The findings differentiate the effects of axonal transport blockade from impulse transmission blockade on nerve enzymes.
- This study provides insights into the biochemical consequences of neurotoxic nerve injury.