Abstract
Purpose: Childhood absence epilepsy (CAE) is an idiopathic form of seizure disorder that is believed to have a genetic basis. Methods: We examined the biophysical consequences of seven mutations in the Cav3.2 T-type calcium channel gene linked to CAE. Results: Of the channel variants examined, one of the mutants, a replacement of glycine 848 in the domain II-S2 region with serine, resulted in significant slowing of the time courses of both activation and inactivation across a wide range of membrane potentials. These changes are consistent with increased channel activity in response to prolonged membrane depolarizations. Conclusions: Taken together, these findings suggest that such little changes in channel gating may contribute to the etiology of CAE.
Original language | English |
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Pages (from-to) | 655-658 |
Number of pages | 4 |
Journal | Epilepsia |
Volume | 47 |
Issue number | 3 |
DOIs | |
Publication status | Published - 1 Mar 2006 |
Externally published | Yes |
Keywords
- calcium channel
- inactivation
- activation
- T-type channels
- epilepsy