Embryonic somatic nerve destruction with beta-bungarotoxin.
The effects and time course of a single injection of beta-bungarotoxin into E14 rat embryos were examined with an electron-microscopic study of development of the internal intercostal somatic nerve. Within 24 h of injection, axons in this nerve became swollen and fused at points along their length. By 48 h after injection no component of the nerve remained in distal segments of ribcage; complete loss of axons and components of the nerve sheath from proximal regions took slightly longer. At later times, no trace of peripheral nerve axons, Schwann cells or elements of the nerve sheath remained. beta-Bungarotoxin applied on E17 destroyed developing axons in a similar manner, but the perineurium remained in place, and axons regenerated within the original nerve trunk. The study confirms that sensory and motor neurons are much less able to survive axon degeneration on E14 than after the major period of normal cell death (which is nearly over by E18), and that the maintenance and continued development of the perineurium during E14-E16 depends on the presence of peripheral nerve axons.
D000818:Animals; D002038:Bungarotoxins / Q000633:toxicity*; D004622:Embryo, Mammalian / Q000187:drug effects; D005314:Embryonic and Fetal Development / Q000187:drug effects; D005260:Female; D008854:Microscopy, Electron; D010525:Peripheral Nerves / Q000196:embryology* / Q000473:pathology / Q000648:ultrastructure; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains
D002038:Bungarotoxins