These R(AB) mice express a transgene containing the cAMP-dependent protein kinase A (PKA or PRKACA) RI alpha regulatory subunit, R(AB) and exhibit a reduction of hippocampal PKA activity with a significant decrease in the late phase of long-term potentiation in the hippocampus.
Ted Abel, University of Pennsylvania
Genetic Background | Generation |
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Allele Type |
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Transgenic (Inserted expressed sequence) |
Mice hemizygous for the transgene are viable and fertile with no gross anatomical abnormalities or structural lesions within the hippocampus or other regions. Transgene expression is observed in hippocampus (CA1, CA3, and dentate gyrus), neocortex, olfactory bulb, striatum, and amygdala. Transgenic mice have a 50% reduction in basal cAMP-dependent protein kinase A (PKA or PRKACA) activity, defective protein synthesis-dependent late phase of long-term potentiation, and reduced place cell stability in hippocampus. Mice have defective long-term, but not short-term, memory in hippocampus-based spatial and non-spatial tasks. This parallels the phenotype observed in mice treated with inhibitors of PKA or inhibitors of protein synthesis. Functional magnetic resonance imaging reveals reduced CA1 hippocampal signal. Transgenic mice are more sensitive to ethanol-induced sedation. Mice expressing this transgene may be useful in a wide variety of memory studies, including Alzheimer's disease, hippocampus-dependent long term memory, protein synthesis-dependent memory, amnesia, or age-related memory decline.
The cAMP-dependent protein kinase A (PKA or PRKACA) RIalpha regulatory subunit, R(AB), was mutated at both cAMP binding sites and placed under control of the mouse Camk2a promoter. The resulting construct was injected into the pronuclei of (B6CBAF1/J x B6CBAF1/J) zygotes. Chimeric males (founder line 426, R(AB)-2) were bred to C57BL/6J females. At some point, hemizygotes were bred to B6CBAF1/J to rescue the line. After the rescue, hemizygotes were bred to C57BL/6J for more than 10 generations before arrival at The Jackson Laboratory.
Expressed Gene | Prkaca, protein kinase, cAMP dependent, catalytic, alpha, mouse, laboratory |
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Site of Expression |
Allele Name | transgene insertion 426, Ted Abel |
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Allele Type | Transgenic (Inserted expressed sequence) |
Allele Synonym(s) | CaMKII-R(AB); R(AB); R(AB)-2 |
Gene Symbol and Name | Tg(Camk2a-Prkaca)426Tabe, transgene insertion 426, Ted Abel |
Gene Synonym(s) | |
Promoter | Camk2a, calcium/calmodulin-dependent protein kinase II alpha, mouse, laboratory |
Expressed Gene | Prkaca, protein kinase, cAMP dependent, catalytic, alpha, mouse, laboratory |
Strain of Origin | (C57BL/6J x CBA/J)F2 |
Chromosome | UN |
Molecular Note | The cAMP-dependent protein kinase A (PKA or PRKACA) RIalpha regulatory subunit, R(AB), was mutated at both cAMP binding sites and placed under control of the mouse Camk2a promoter. |
Mutations Made By | Ted Abel, University of Pennsylvania |
When maintaining a live colony, hemizygotes are bred to wildtype siblings or to inbred C57BL/6J mice.
When using the R(AB) mouse strain in a publication, please cite the originating article(s) and include JAX stock #005855 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Hemizygous or Non carrier for Tg(Camk2a-Prkaca)426Tabe |
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