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© 1984 Oxford University Press

research-article

Soman Induced Changes in Brain Regional Glucose Use1

FRED E. SAMSON, THOMAS L. PAZDERNIK, ROBERT S. CROSS, MARY P. GIESLER, KLAUS MEWES, STANLEY R. NELSON and JOHN H. MCDONOUGH*

Departments of Pharmacology, Toxicology, and Therapeutics, Anatomy and Physiology, and the Ralph L. Smith Research Center, University of Kansas Medical Center Kansas City, Kansas 66103 *U.S. Army Medical Research Institute of Chemical Defense Aberdeen Proving Ground, Maryland 21010

Soman Induced Changes in Brain Regional Glucose Use. SAMSON F. E., PAZDERNIK, T. L., CROSS, R. S., GIESLER, M. P., MEWES, K., NELSON, S. R., AND MCDONOUGH, J. H. (1984). Fundam. Appl. Toxicol. 4, S173–S183. Soman, a potent central acetylcholine esterase inhibitor, has a greater impact on brain regional glucose use than other organophosphates, such as diiso-propylfluorophosphate (DFP) or phospholinium iodide. At near-lethal doses soman induced explosive persistent seizures that were associated with a greater than fourfold increase of glucose use in many brain structures. Single near-lethal doses of soman lead to conspicuous neuronal damage and a marked reduction in brain activity, 1 to 3 days after exposure. When soman (2 x LD50) was given to TAB (an antidotal mixture of trimedoxime, atropine, and benactyzine) pretreated rats, there was a greater than twofold reduction of glucose use in almost every brain region. We suggest that soman seizures are mediated via activation of muscarinic receptors; also, the substantia nigra has a key role in the initiation/propagation of seizures. Soman has in addition, a depressive effect on some brain components which appears not to involve muscarinic receptors. We suggest that the conspicuous pathology that follows a single, near-lethal dose of soman results from a depletion of energy flow along with an influx of Ca2+ which sets into motion a cascade of destructive reactions, such as activation of proteases.


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