Aberrant reduction of an inhibitory protein factor in a rat epileptic model

Amano, Taku; Matsubayashi, Hiroaki; Özkan, Eric D.; Sasa, Masashi; Serikawa, Tadao; Ueda, Tetsufumi

doi:10.1016/s0920-1211(02)00122-5

Cited by 2 publications

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“…In addition to abnormalities of the Ca 2+ channels described above, functional alterations induced by repeated seizures in SER were also studied in GABA A receptor [ 25 ], benzodiazepine receptor [ 101 ], NMDA receptor [ 71 ], muscarinic cholinergic receptor [ 75 ], and voltage-gated sodium channels subtypes [ 30 ], and for contents of neuropeptides [ 92 , 105 ]. Aberrant reduction in inhibitory protein factor (IPF), which potently inhibits glutamate uptake into synaptic vesicles, was found in hippocampus of aged SER, suggesting the seizures are involved in excessive glutamate transmission [ 8 ]. Although SER exhibit retardation in learning ability, their poor operant performance was improved by continual intake of PB in the rats [ 10 ], suggesting the importance of seizure control.…”

Section: Canavan-disease Related Epileptic Models: Trm and Sermentioning

confidence: 99%

Advances on genetic rat models of epilepsy

et al. 2015

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Considering the suitability of laboratory rats in epilepsy research, we and other groups have been developing genetic models of epilepsy in this species. After epileptic rats or seizure-susceptible rats were sporadically found in outbred stocks, the epileptic traits were usually genetically-fixed by selective breeding. So far, the absence seizure models GAERS and WAG/Rij, audiogenic seizure models GEPR-3 and GEPR-9, generalized tonic-clonic seizure models IER, NER and WER, and Canavan-disease related epileptic models TRM and SER have been established. Dissection of the genetic bases including causative genes in these epileptic rat models would be a significant step toward understanding epileptogenesis. N-ethyl-N-nitrosourea (ENU) mutagenesis provides a systematic approach which allowed us to develop two novel epileptic rat models: heat-induced seizure susceptible (Hiss) rats with an Scn1a missense mutation and autosomal dominant lateral temporal epilepsy (ADLTE) model rats with an Lgi1 missense mutation. In addition, we have established episodic ataxia type 1 (EA1) model rats with a Kcna1 missense mutation derived from the ENU-induced rat mutant stock, and identified a Cacna1a missense mutation in a N-Methyl-N-nitrosourea (MNU)-induced mutant rat strain GRY, resulting in the discovery of episodic ataxia type 2 (EA2) model rats. Thus, epileptic rat models have been established on the two paths: ‘phenotype to gene’ and ‘gene to phenotype’. In the near future, development of novel epileptic rat models will be extensively promoted by the use of sophisticated genome editing technologies.

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