Homozygous leaner mice carry an autosomal recessive mutation in the Ca2+ channel subunit gene, α(1A), causing them to exhibit severe ataxia, petit-mal-like epilepsy and a myoclonus-like movement disorder. Expression of α(1A) mRNA in cerebella from 20-day-old homozygous leaner mice was compared to control mice, using in situ hybridization histochemistry. Expression of α(1A) protein was examined in cerebella from 20-day-old homozygous leaner and control mice using immunocytochemistry. No differences in either mRNA or protein expression of the α(1A) subunit were observed when homozygous leaner mice were compared to age-matched controls. Therefore, functional alterations in P/Q-Type Ca2+ channels containing the α(1A) subunit need to be explored to further understand the relationship of mutations in the α(1A) gene to the pathogenesis of the neurologic disorders occurring in leaner mice.
- Cerebellar granule cell
- In situ hybridization histochemistry
- Ion channel mutation
- Purkinje cell
ASJC Scopus subject areas
- Molecular Biology
- Cellular and Molecular Neuroscience