Neuroprotective activity of glutamate receptor antagonists against soman-induced hippocampal damage: quantification with an ω3 site ligand
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Cited by (64)
Cerebral blood flow and oxygenation in rat brain after soman exposure
2021, Toxicology LettersCitation Excerpt :Treatment protocols involve attenuation of peripheral symptoms and prevention of convulsive seizures (Barker et al., 2020; Sidell, 1998). However, current treatments are unable to provide neuroprotection unless seizures are quickly terminated (Baille et al., 2005; Lallement et al., 1993). It is accepted that exposure to NAs causes neurological damage (Philippens et al., 1992).
Assessment of brain oxygenation imbalance following soman exposure in rats
2018, NeuroToxicologyCitation Excerpt :In other studies, either through innate tolerance or anti-seizure medication, in the absence of convulsive seizures, no neurological degeneration was observed (Apland et al., 2010; Baille et al., 2005; Guo et al., 2015; Lallement et al., 1993; McDonough et al., 1987). When convulsive seizures were terminated within 20 min, minimal neuronal loss was seen (Baille et al., 2005; Lallement et al., 1993), indicating the presence and duration of seizures to be a critical factor in soman related neurological damage. Seizures induced by soman (Shih and McDonough, 1997) cause neurological damage through excitotoxicity (Fujikawa et al., 2000; Lallement et al., 1993; Olney et al., 1974).
General Overview
2014, Best Synthetic Methods: Organophosphorus (V) ChemistryCyclooxygenase-2 contributes to VX-induced cell death in cultured cortical neurons
2012, Toxicology LettersCitation Excerpt :When this enzyme is inhibited, there is an accumulation of the neurotransmitter in the synaptic cleft resulting, for doses that are sufficient, in the progression of toxic signs including hypersecretions, tremors, convulsions, respiratory distress and ultimately death (Weinbroum, 2005). Glutamate receptors are thought to participate in the propagation and maintenance of OP-induced seizures and to play a major role in mediating the CNS neurotoxicity of OP nerve agent after seizures (e.g. Lallement et al., 1993; Solberg and Belkin, 1997). It has been suggested that the glutamate released by nerve agent exposure plays a role in mediating neuronal death following OP-induced CNS intoxication (e.g. McDonough and Shih, 1997; Lallement et al., 1992; Solberg and Belkin, 1997).
Nerve agent intoxication: Recent neuropathophysiological findings and subsequent impact on medical management prospects
2011, Toxicology and Applied PharmacologyCitation Excerpt :Indeed, from post-soman day 4 to post-soman day 22, the number of monocytes and granulocytes in the blood circulation had considerably increased (Collombet et al., 2005a). Phagocytic events involving activated monocytes (invading macrophages) and granulocytes are required in damaged brain regions to remove accumulated cell debris, as suggested by the macrophage invasion already observed in wounded brain regions 1, 2 and 7 days after soman exposure (Baille et al., 2005; Lallement et al., 1993). The extensive need for activated monocytes and granulocytes in the brain could contribute to further cell quantity increase in blood (Fig. 2).