
It is clear that a variety of gene defects can result in absence seizures. In addition, the problem is complicated by observation that the behavioral and EEG phenotype in some of the models is highly dependent on pedigree. Despite these difficulties, advances in molecular-genetic techniques coupled with electrophysiological studies are likely to be highly revealing. While the relationship between the rat and mice models and the human condition thus far remains tenuous, insights from the animal models have already been very helpful in choosing antiepileptic drugs and providing insights into the pathophysiology of the seizures.
Receptors, GABA-A, Mice, Mutant Strains, Rats, Mutant Strains, Rats, Disease Models, Animal, Mice, Epilepsy, Absence, Seizures, Animals, Humans, Calcium Channels
Receptors, GABA-A, Mice, Mutant Strains, Rats, Mutant Strains, Rats, Disease Models, Animal, Mice, Epilepsy, Absence, Seizures, Animals, Humans, Calcium Channels
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