Abstract：
:Mutations at the mouse tottering (tg) locus cause a delayed-onset, recessive neurological disorder resulting in ataxia, motor seizures, and behavioral absence seizures resembling petit mal epilepsy in humans. A more severe allele, leaner (tg(la)), also shows a slow, selective degeneration of cerebellar neurons. By positional cloning, we have identified an alpha1A voltage-sensitive calcium channel gene that is mutated in tg and tg(la) mice. The alpha1A gene is widely expressed in the central nervous system with prominent, uniform expression in the cerebellum. alpha1A expression does not mirror the localized pattern of cerebellar degeneration observed in tg(la) mice, providing evidence for regional differences in biological function of alpha1A channels. These studies define the first mutations in a mammalian central nervous system-specific voltage-sensitive calcium channel and identify the first gene involved in absence epilepsy.
journal_name
Celljournal_title
Cellauthors
Fletcher CF,Lutz CM,O'Sullivan TN,Shaughnessy JD Jr,Hawkes R,Frankel WN,Copeland NG,Jenkins NAdoi
10.1016/s0092-8674(00)81381-1subject
Has Abstractpub_date
1996-11-15 00:00:00pages
607-17issue
4eissn
0092-8674issn
1097-4172pii
S0092-8674(00)81381-1journal_volume
87pub_type
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