B6;129P2-Prkcg^tm1Stl/J

Stock number: 002466
Product name: PKCγ KO
Research areas: Neurobiology Research, Sensorineural Research

Description

These Prkcg knock-out mice exhibit diminished long-term potentiation in the hippocampus. They are suitable for use in applications related to the study of long-term potentiation in neuron signal transmission.

Detailed description

Mice homozygous for the Prkcg^tm1Stl targeted mutation are viable and develop normally. Homozygous mice show diminished long-term potentiation (LTP) in the hippocampus, but two other types of synaptic plasticities are normal, namely long-term depression and paired-pulse facilitation. Despite this diminished LTP capacity homozygotes can learn to do hippocampus-dependant tasks, such as the Morris water maze and context-dependent fear conditioning, with only slight deficits.

Development

The Prkcc deficient strain was developed in the lab of Dr. Susumu Tonegawa at the Center for Cancer Research at the Massachusetts Institute of Technology. The 129-derived E14 ES cell line was used.

Allele

Symbol: Prkcg^tm1Stl
Name: targeted mutation 1, Susumu Tonegawa
MGI accession ID: MGI:1857237
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: PKCgamma-KO
Marker symbol: Prkcg
Marker name: protein kinase C, gamma
Marker synonyms: PKC; Pkcc; PKCG; PKCgamma; PKC-gamma; PKCI; PKCI(3); Prkc; Prkcc; RATPKCI; SCA14
Chromosome: 7
Strain of origin: 129P2/OlaHsd
Molecular note: A neomycin resistance cassette replaced 2.5kb of sequence containing the exon that encodes the nucleotide binding domain. Northern blot analysis of total brain RNA demonstrated that homozygous mutant mice lack normal transcripts. Western blot analysis of total brain protein did not detect the protein in homozygous mutant mice.