Residual acetylcholinesterase activity in the basal lateral amygdala following soman-induced status epilepticus

Soman (pinacolylmethylphosphonofluoridate) causes seizures and seizure-rela ted brain damage resulting from the ir reversible inhibition of acetylcholi nesterase (AChE) in the central nervous system (CNS). The authors have exam ined the possibility that the loss of AChE reactivity in discrete brain reg ions may have importance in the development of status epilepticus caused by soman. In these studies, male Sprague-Dawley rats were given GM(1) monosia loganglioside, intracerebroventricularly, via an osmotic minipump. Four day s after initiation of GM(1) infusions, rats were injected with 2.25 LD50 so man (83 mu g/kg, im). Electrocorticogram (ECoG) recordings were monitored v ia indwelling cortical electrodes. All rats were euthanized 27 h after soma n administration. Brain tissue was sucrose-saturated, cryostat-sectioned, a nd processed for AChE histochemistry. A Quantimet 600 Image Analysis System and Biological Microscope were used to assess the optical density of histo chemical staining for AChE in the piriform cortex, basolateral amygdaloid n ucleus, and caudate putamen. All rats showed ECoG evidence of seizures with in 10 min of soman administration. However, 6 of the 11 surviving rats rece iving GM(1) infusion did not develop status epilepticus. Statistical analys is of AChE optical densities revealed marked and significant reductions of AChE reactivity in soman-treated rats compared to controls. Soman-treated r ats that did not develop status epilepticus had significant levels of resid ual AChE in, the basolateral amygdaloid nucleus compared to other soman-cha llenged animals.