Origin
Komeda Zucker Creeping rat derived from a closed colony of the Zucker fatty rat by spontaniously mutation at Tokyo Medical College in 1983.
Strain characteristics
The animals exhibiting severe ataxia with staggering gait and tremor at about 14 days of age, and die around 4 weeks of age. The cerebellum of the mutants shows severe hypoplasia with the reduction of the molecular and granular layers and malposition of Purkinje cells in the white matter. The abnormal pathological changes are also detected in the cerebrum, including the absence of a well-defined outer molecular layer, no typical lamination, and irregular cell arrangement in the hippocampus.
Breeding Conditions
Homozygous Reln rats are difficult to breed. Maintained in heterozygous condition.
Genotyping
One base insertion detected by PCR-direct sequencing.
References
Nakanishi S, Kuramoto T, Kashiwazaki N, Yokoi N.
Genetic profiling of two phenotypically distinct outbred rats derived from a colony of the Zucker fatty rats maintained at the Tokyo Medical University.
Exp Anim. 2016 Oct 31. [Epub ahead of print]
Yokoi N, Namae M, Wang HY, Kojima K, Fuse M, Yasuda K, Serikawa T, Seino S, Komeda K.
Rat neurological disease creeping is caused by a mutation in the reelin gene.
Brain Res Mol Brain Res. 10;112(1-2):1-7, 2003.
Yokoi N, Shimizu S, Ishibashi K, Kitada K, Iwama H, Namae M, Sugawara M, Serikawa T, Komeda K.
Genetic mapping of the rat mutation creeping and evaluation of its positional candidate gene reelin.
Mamm Genome. 11(2):111-4, 2000.
Ishibashi K, Komeda K, Sekiguchi F, Kanazawa Y.
Creeping: a new mutant rat with neurological disease.
Lab Anim Sci. 39(2):132-6, 1989.