“…Dendritic degeneration seen in this model of DFP-induced seizures is similar to neurodegeneration of pyramidal neurons in CA1 hippocampal area in mouse models of kainic acid (KA)-induced excitotoxicity (Zaja-Milatovic et al, 2008) and activated innate immunity (Milatovic et al, 2003 OPIDN has been attributable to inhibition of neuropathy target esterase (NTE), rather than AChE, as inhibition of AChE is not necessary for the development of OPIDN (Pope et al, 1993;Wu and Casida, 1996;Jamal, 1997). Hence, since nerve agents target AChE much more than NTE (Gordon et al, 1983), the degree to which OPIDN would emerge as a significant consequence of nerve agent exposure alone is questionable; rather, doses that could potentially lead to OPIDN would, as a practical matter, cause lethal acute anti-AChE effects first. As a practical matter, unlike many other OPs, VX has not been shown to induce OPIDN and is reported to be at least 1,000 times less effective than sarin in inhibiting NTE (Gordon et al, 1983).…”