| First Author | Kim TY | Year | 2016 |
| Journal | Exp Anim | Volume | 65 |
| Issue | 3 | Pages | 207-14 |
| PubMed ID | 26887908 | Mgi Jnum | J:278031 |
| Mgi Id | MGI:6356085 | Doi | 10.1538/expanim.15-0120 |
| Citation | Kim TY, et al. (2016) Protein expression pattern in cerebellum of Cav2.1 mutant, tottering-6j mice. Exp Anim 65(3):207-14 |
| abstractText | Neuronal voltage-gated Cav2.1 channel controls a broad array of functions, including neurotransmitter release, neuronal excitability, activity-dependent gene expression, and neuronal survival. The Cav2.1 channel is molecular complexes consisting of several subunits: alpha1, alpha2/delta, beta, and gamma. The pore-forming subunit, alpha1, is encoded by the Cacna1a gene. Tottering-6j mice, generated by the Neuroscience Mutagenesis Facility at The Jackson Laboratory, are a recessive mutant strain in which the mutation has been chemically induced by ethylnitrosourea. In tottering-6j mice, mutation in the Cacna1a gene results in a base substitution (C-to-A) in the consensus splice acceptor sequence, which results in deletion of a part of the S4-S5 linker, S5, and a part of S5-S6 linker domain I in the alpha1 subunit of Cav2.1 channel. The mice display motor dysfunctions and absence-like seizures. However, protein expression in the cerebellum of tottering-6j mice has not been investigated. Real-time quantitative reverse transcription polymerase chain reaction and histological analyses of the cerebellum of tottering-6j mice revealed high expression levels of tyrosine hydroxylase, zebrin II, and ryanodine receptor 3 compared with those of wild-type mice. Conversely, a low level of calretinin expression was found compared with wild-type mice. These results indicate that Cacna1a mutation plays a significant role in protein expression patterns and that the tottering-6j mouse is a useful model for understanding protein expression mechanisms. |
