Effects of soman-induced seizures on different extracellular amino acid levels and on glutamate uptake in rat hippocampus

The effects of repeated low-dose sarin exposure☆

“…An increase in dopamine metabolites, i.e., 3,4-dihydroxyphenylacetic (DOPAC) and homovanillic acid (HVA), is evident approximately 10 minutes after seizure onset with increases in HVA continuing for up to 80 minutes after seizure onset McDonough and Shih, 1997). Increases in extracellular glutamate have also been reported in numerous brain regions following soman-induced seizure onset (Lallement et al, 1991). These data, taken together, support the idea that there is a triphasic NT model for onset and progression of seizures and subsequent brain damage upon acute exposure to OP ChE inhibitors .…”

Histomorphogenesis of Soman-Induced Encephalocardiomyopathy in Sprague-Dawley Rats

“…This finding was surprising because there is some evidence to suggest that acetylcholine is a retinal neurotransmitter (52) and that soman neurotoxicity is partly attributed to recruitment of glutamatergic synapses (16,37,38,41), which are also known to occur in the retina. Additional work with different doses of soman will be needed to address this issue.…”

“…Recently it was suggested that neither the nerve agent-induced seizure activity per se nor the direct toxic actions of the nerve agent appear to be responsible for the nerve agent induced neuropathology, supporting the coparticipation of a noncholinergic mechanism (29,36,37,(39)(40)(41)45). However, as the hypothesis on the soman-induced neuropathology evolved, the effects of the endogenous excitatory amino acids in soman-induced seizures (8,37,40) and intracellular calcium overload have been implicated as causative agents in the death of the cells. Cardiac damage, an associated lesion, is thought to be neurogenic in origin ( 19,44,59,66,69).…”

The M1 Muscarinic Receptor Antagonist VU0255035 Delays the Development of Status Epilepticus after Organophosphate Exposure and Prevents Hyperexcitability in the Basolateral Amygdala

“…Therefore, the absence of a significant effect of the VU0255035 pretreatment during the first 10 minutes is probably not attributable to a delay of the drug reaching the brain. Other mAChR subtypes may be involved in the generation of seizure activity at this early phase, or an increase of glutamate may be the culprit, since extracellular glutamate has been found to increase in the amygdala within the first 10 minutes after exposure to soman (Lallement et al, 1991). During the next 30 minutes (after the initial 10-minute period), the M 1 antagonist in the VU0255035-treated group prevented SE (stage 3 and higher), but seizures below stage 3 were ongoing; again, other mAChR subtypes and/or glutamatergic mechanisms may be involved in sustaining low-intensity seizures during this postexposure period.…”