Establishment Of An Epilepsy Model Induced By Sodium Fluoroacetate In Rats And Research On Its Mechanism

Epilepsy is a recurrent neurological syndrome. It is difficult to cure completely because of its complicated and unclear pathogenesis. Establishing an animal model of epilepsy is an important tool for researching on the mechanism of epilepsy and screening anti-epileptic drugs. Nowadays, as more and more attention are paid to glia, which is considered to play an important role in epileptic pathogenesis,In this study, we chose fluoroacetate, a reversible neuroglia metabolic inhibitor as well as a rodenticide that can induce epileptic seizures, to set up a new epileptic animal model by acting on neuroglia to induce seizures. Such a model is evaluated by paraxiology and electrophsiology. We also studied its pacemaker and route of transmission with Fos protein immunohistochemical method, and observed glial functional changes, relationship between glia and neuron before and after seizure, andpathological changes in frontal cortex and hippocampus.Results:?Fluoroacetate can induce generalized seizures in rats stably and a typical EEG alteration. (2) Fluoroacetate induces protein express in orders, first in ebtorhinal cortex, piriform cortex, hippocampus, and then in amygdaloid nucleus limbic system and cortices, (D Fluoroacetate can reduce the expression of GEAR ?Extensive pathological damage appears in frontal cortex and hippocampus after the injection of f luoroacetate, this damage reaches the highest level at 24 h and especially serious in hippocampus, while the ghVs damage isn't obvious.Conclusions: (D The model of fluoroacetate inducing epileptic seizure is a convenient > stable forebrain epilepsy model, in accordant with clinic pathology. @ The route of transmission may be from entorhinal cortex and piriform cortex to cortices and limbic system such as hippocampus, amygdaloid nucleus et al. (3) The mechanism of fluoroacetate inducing seizure may be through restraining glial function, and the dose of 3mg/kg can only induce glial function change, but not the irreversible pathological damage. (4) Extensive pathological damage appears in frontal cortex and hippocampus after the injection of fluoroacetate, this damage reaches the highest level at 24 h and especially serious in hippocampus, while the glia's damage isn't obvious.?The fluoroacetate epilepsy model established in present study provides a new tool for studying glial role in epileptic mechanism and relationship between glia and neuron.