Involvement of Lipid Metabolism in the Action of Phospholipase A2 Neurotoxins
Abstract
Presynaptically-acting neurotoxins (PSNTXs) from snake venom irreversibly stimulate acetylcholine (ACh) release from and inhibit choline uptake into synaptosomes, with rat synaptosomes affected by more toxins than those from mice. The inclusion of BSA in the incubation medium at the time of toxin expose has allowed a clear distinction to be made between nonPSNTX phospholipases A2 (PLA2s) and the PSNTXs in synaptosome preparations. The stimulation of ACh release by scutoxin and pseudexin, but not by Beta- bungarotoxin (Beta-Butx), was antagonized only by neutralizing antibodies to pseudexin. The PSNTXs exhibit a pattern of phospholipid hydrolysis different from nonPSNTX PLA2s, as determined either by type of fatty acid liberated, or by the type of phospholipid hydrolyzed. This PLA2 activity may play a role in neurotoxicity. PSNTXs (Beta-Butx), cardiotoxins (CTXs), melittin and myotoxin alpha all cause Ca(2+) release from the terminal cisternae of the sarcoplasmic reticulum through the Ca(2+) release channel. Melittin and CTX, but not PSNTXs or myotoxin alpha, activate phospholipase C activity with no requirement for extracellular Ca(2+).
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 03, 1993
- Accession Number
- ADA277284
Entities
People
- Jeffrey E. Fletcher