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• W1738059634 endingPage "4489" @default.
• W1738059634 startingPage "4482" @default.
• W1738059634 abstract "Mutations of the α_1A calcium channel subunit have been shown to cause such human neurological diseases as familial hemiplegic migraine, episodic ataxia-2, and spinocerebellar ataxia 6 and also to cause the murine neurological phenotypes of<i>tottering</i> and <i>leaner</i>. The<i>leaner</i> phenotype is recessive and characterized by ataxia with cortical spike and wave discharges (similar to absence epilepsy in humans) and a gradual degeneration of cerebellar Purkinje and granule cells. The mutation responsible is a single-base substitution that produces truncation of the normal open reading frame beyond repeat IV and expression of a novel C-terminal sequence. Here, we have used whole-cell recordings to determine whether the<i>leaner</i> mutation alters calcium channel currents in cerebellar Purkinje cells, both because these cells are profoundly affected in <i>leaner</i> mice and because they normally express high levels of α_1A. In Purkinje cells from normal mice, 82% of the whole-cell current was blocked by 100 nmω-agatoxin-IVA. In Purkinje cells from homozygous<i>leaner</i> mice, this ω-agatoxin-IVA-sensitive current was 65% smaller than in control cells. Although attenuated, the ω-agatoxin-IVA-sensitive current in homozygous <i>leaner</i>cells had properties indistinguishable from that of normal Purkinje neurons. Additionally, the ω-agatoxin-IVA-insensitive current was unaffected in homozygous <i>leaner</i> mice. Thus, the<i>leaner</i> mutation selectively reduces P-type currents in Purkinje cells, and the α_1A subunit and P-type current appear to be essential for normal cerebellar function." @default.
• W1738059634 created "2016-06-24" @default.
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• W1738059634 date "1998-06-15" @default.
• W1738059634 modified "2023-10-03" @default.
• W1738059634 title "Altered Calcium Channel Currents in Purkinje Cells of the Neurological Mutant Mouse<i>leaner</i>" @default.
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• W1738059634 doi "https://doi.org/10.1523/jneurosci.18-12-04482.1998" @default.
• W1738059634 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6792698" @default.
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