Recovery from soman-induced hypothermia is due to an increase in acetylcholinesterase activity but not new protein synthesis

Neurotoxicology. 1993 Winter;14(4):411-6.

Abstract

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.

MeSH terms

  • Acetylcholinesterase / drug effects*
  • Animals
  • Body Temperature Regulation / drug effects*
  • Cycloheximide / pharmacology*
  • Hypothalamus, Anterior / drug effects*
  • Hypothalamus, Anterior / enzymology
  • Male
  • Mice
  • Protein Biosynthesis*
  • Soman

Substances

  • Soman
  • Cycloheximide
  • Acetylcholinesterase