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In Vitro
Journal Article
Research Support, Non-U.S. Gov't
Functional analysis of Ca3.2 T-type calcium channel mutations linked to childhood absence epilepsy.
Epilepsia 2006 March
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 Ca(v)3.2 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.
METHODS: We examined the biophysical consequences of seven mutations in the Ca(v)3.2 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.
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