The neurotoxicological effects of mastoparan Polybia-MPII at the murine neuromuscular junction: an ultrastructural and immunocytochemical study

• Published in: Histochemistry and cell biology 2009-10, Vol.132 (4), p.395-404
• Main Authors: Rocha, Thalita, de Souza, Bibiana M., Palma, Mario S., da Cruz-Höfling, Maria Alice, Harris, John Buchanan
• Format: Article
• Language: English
• Subjects: Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Bungarotoxins - metabolism; Cell Biology; Cellular biology; Cholinesterases - metabolism; Developmental Biology; Histology; Hymenoptera; Injections, Intramuscular; Male; Mice; Microscopy, Electron, Transmission; Mitochondria - drug effects; Mitochondria - ultrastructure; Muscle, Skeletal - drug effects; Muscle, Skeletal - enzymology; Muscle, Skeletal - ultrastructure; Neuromuscular Junction - drug effects; Neuromuscular Junction - ultrastructure; Neurotoxins - toxicity; Original Paper; Peptides - toxicity; Polybia paulista; Receptors, Nicotinic - metabolism; Rhodamines - metabolism; Rodents; Synaptic Vesicles - drug effects; Synaptic Vesicles - ultrastructure; Synaptophysin - metabolism; Toxicology; Wasp Venoms - toxicity; Wasps - chemistry
• ISSN: 0948-6143; 1432-119X
• DOI: 10.1007/s00418-009-0607-z

Polybia-MPII (INWLKLGKMVIDAL-NH 2 ), a mastoparan isolated from the crude venom of the swarming wasp Polybia paulista , was injected into the left hind limb of Swiss white mice. Between 3 h and 21 days later the mice were killed and the soleus muscles from both hind limbs were removed. Sections of the muscles were made for transmission electron microscopy and immunocytochemistry. Transmission electron microscopy showed that both the volume fraction occupied by synaptic vesicles and synaptic vesicle density was greatly reduced after exposure to Polybia-MPII, although there was no significant structural damage to the plasma membrane of the terminal boutons and mitochondria were indistinguishable from those in normal, control boutons. Immunocytochemistry revealed that in control muscles 99% of motor end plates identified by the positive labelling of acetylcholine receptors by TRITC-α-bungarotoxin co-labelled with anti-synaptophysin antibody, but this figure fell by 30% in muscles exposed to the toxin. These changes were transient. They were maximal at 6 h and fully reversed by 3 days. At no time was axonal labelling with anti-neurofilament antibodies affected by exposure to Polybia-MPII. We conclude that mastoparan Polybia-MPII is a minor neurotoxin and suggest that its neurotoxic activity is unlikely to be of clinical significance.