Seizures anti-AChE-induced

ANTI-ACHE-INDUCED SEIZURES, OXIDATIVE INJURY, AND NEURODEGENERATION... 

Time-course changes in biomarkers of oxidative damage in the rat model of anti-AChE-induced seizures showed that the highest increase in F2-IS0PS was... 

In conclusion, the data demonstrated that synergistic mechanisms of cellular disruption caused by anti-AChE agents led to cellular dysfxmction and neurodegeneration. It has also been demonstrated that preventing CF-induced neuronal hyperactivity by pretreatment with memantine and atropine blocks pathways associated with oxidative damage in rat brain. The documented ability of memantine therapy to reduce free radical generation and lipid peroxidation, prevent HEPs, and attenuate the morphological injury provides further support for the role of ROS and RNS in anti-AChE-induced seizures. 

Of the five known classes of muscarinic ACh receptors, M-current is preferentially inhibited by m 1 or m3 subtypes (515,516). Experiments with mice lacking the m 1 receptor exhibit a loss of muscarinic regulation of M-current and are resistant to pilocarpine-induced seizures (517). Recently, specific anti-sense plasmids have been used to strongly suggest the G-protein as the primary transducer of muscarinic inhibition of /rcm) (518). 

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