Recovery from soman-induced hypothermia is due to an increase in acetylcholinesterase activity but not new protein synthesis.
Organophosphate-induced hypothermia in rodents appears to be due to stimulation of muscarinic receptors in the anterior hypothalamus. The nerve agent soman (pinacolyl methylphosphonofluoridate) produced a transient hypothermia in mice. Concomitant with the recovery from soman-induced hypothermia, which was complete within 6 hr, there was a parallel recovery of the hypothalamic acetylcholinesterase activity. Pretreatment of mice with the protein synthesis inhibitor, cycloheximide, did not affect the recovery from soman-induced hypothermia nor the recovery of hypothalamic acetylcholinesterase activity. The results suggest that the recovery from soman-induced hypothermia may be due to the recovery of acetylcholinesterase, perhaps from the assembly of previously synthesized precursors.
Clement
J G
JG
Biomedical Defence Section, Defence Research Establishment Suffield, Ralston, Alta., Canada.
D000110:Acetylcholinesterase / Q000187:drug effects*; D000818:Animals; D001833:Body Temperature Regulation / Q000187:drug effects*; D003513:Cycloheximide / Q000494:pharmacology*; D007032:Hypothalamus, Anterior / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D051379:Mice; D014176:Protein Biosynthesis; D012999:Soman
D012999:Soman; D003513:Cycloheximide; D000110:Acetylcholinesterase