Abstract
An animal model of human absence epilepsy containing a G to C mutation of the Cav3.2 T-type Ca2+ channel gene (Cacna1h) ties together the gene mutation, increased T-type Ca2+ channel activity and the epileptic phenotype. Mice lacking a related gene (Cacna1a) also show enhanced T-type Ca2+ current and increased susceptibility to absence seizures. On the other hand, mutations that decrease T-type Ca2+ channel activity in thalamocortical relay neurons display no spike–wave discharges associated with absence seizures. These animal models are supported by genetic studies showing defects in T-type Ca2+ channel function in humans suffering from epilepsy. Thus, in both human and animal studies, T-type Ca2+ channel antagonists show promise in the treatment of absence seizures.
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Acknowledgements
We thank Peggy Mankin and Hongyi Chen for manuscript preparation. This work was funded by the Pediatrics Department fund, Children’s Hospital of Illinois.
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Chen, Y., Parker, W.D. (2015). Link Between Absence Seizures and T-Type Calcium Channels. In: Schaffer, S., Li, M. (eds) T-type Calcium Channels in Basic and Clinical Science. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1413-1_7
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DOI: https://doi.org/10.1007/978-3-7091-1413-1_7
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