The Genetically Epilepsy-Prone Rat: Neuronal Networks And Actions Of Amino Acid Neurotransmitters

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Abstract
The genetically epilepsy-prone rat (GEPR) is a naturally occurring epilepsy model that was originally derived from the Sprague-Dawley strain of rats at the Universities of Arizona and Louisiana State. 1 The antecedent AGS-susceptible rats (GEPR-antecedent) from which the GEPR-9 is descended exhibited variable and inconsistent degrees of seizure severity. The GEPR-antecedent strains are no longer available. The GEPR has been described fully in the previous chapter by Jobe and co-workers. This model exhibits a genetic predisposition to epilepsy with evidence suggesting that inheritance of the audiogenic seizure trait is polygenetic and autosomal dominant. 13 Genetic predisposition is also an important factor in many forms of human epilepsy. 2 The GEPR exhibits audiogenic seizures (AGS) in response to high intensity acoustic stimuli, and this animal also displays an elevated sensitivity to convulsant drugs, kindling, electroshock, hyperbaric, and hyperthermic seizures 1 (see below). Neurotransmitter abnormalities have been observed in the GEPR that may be important in AGS susceptibility. The GEPR exhibits widespread deficits of brain norepinephrine and 5-hydroxytryptamine, and these neurotransmitters are both commonly associated with neuronal and seizure inhibition. 1 Recent evidence indicates that alterations of both excitant and inhibitory amino acids are important in initiation mechanisms for AGS in the GEPR. The evidence obtained, thus far, supports increases in levels of excitant amino acids and increases in amounts but decreased efficacy of GABA in the inferior colliculus of the GEPR. The deficit of hearing that occurs in these animals also appears to be an important underlying element, which may lead to audiogenic seizure susceptibility in the GEPR.

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