Expression of calcium channel α1A mRNA and protein in the leaner mouse (tgla/tgla) cerebellum

Homozygous leaner mice carry an autosomal recessive mutation in the Ca2+ channel subunit gene, alpha(1A), causing them to exhibit severe ataxia, petit-mal-like epilepsy and a myoclonus-like movement disorder. Expression of alpha(1A) mRNA in cerebella from 20-day-old homozygous leaner mice was compared to control mice, using in situ hybridization histochemistry. Expression of alpha(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 alpha(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 alpha(1A) subunit need to be explored to further understand the relationship of mutations in the alpha(1A) gene to the pathogenesis of the neurologic disorders occurring in leaner mice. (C) 1998 Elsevier Science B.V. All rights reserved.