Trpc5 (transient receptor potential cation channel, c5) knockout mice exhibit resistance to pilocarpine-induced seizures, minimal seizure-induced neuronal cell death, and reduced long term potentiation.
Lutz Birnbaumer, National Institutes of Health
Trpc5 (transient receptor potential cation channel, c5) encodes a multi-pass membrane protein that forms a receptor-activated cation channel. Homozygous knockout mice exhibit resistance to pilocarpine-induced seizures (in the late phase), minimal seizure-induced neuronal cell death in the hippocampus, and reduced long term potentiation. This strain may be useful for studying epileptogenesis and neuronal excitotoxicity.
The targeting vector contains a loxP site inserted upstream of exon 5 and a loxP site inserted downstream of exon 5. In the protein this results in the loss of the transmembrane 5 pore and transmembrane 6 ion channel domain. The construct was electroporated into 129S6/SvEvTac-derived embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. The resulting chimeric animals were interbred and offspring were crossed to B6.Cg-Tg(Sox2-cre)1Amc/J mice to remove exon 5. Offspring were interbred to generate a homozygous colony. Upon arrival, mice were bred to C57BL/6J for at least 1 generation to establish the colony.
|Allele Name||targeted mutation 1.1, Lutz Birnbaumer|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Trpc5, transient receptor potential cation channel, subfamily C, member 5|
|Strain of Origin||129S6/SvEvTac|
|Molecular Note||Exon 5 was floxed via homologous recombination. Cre mediated recombination removed exon 5. Absence of protein expression was confirmed by immunofluorescent staining of the hippocampal region of homozygous mice.|
While maintaining a live colony, these mice carrying this X-linked allele are bred as homozygote female to hemizygous male.
When using the STOCK Trpc5tm1.1Lbi/Mmjax mouse strain in a publication, please cite the originating article(s) and include MMRRC stock #37349 in your Materials and Methods section.