MGI phenotypes (allele matching)
B6.129-Kcnab1tm1Sva/Ieg
| Status | Available to order |
| EMMA ID | EM:06228 |
| Citation information | RRID:IMSR_EM:06228 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | B6.129-Kcnab1tm1Sva/Ieg |
| Alternative name | B6.129-Kcnab1 |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Kcnab1tm1Sva |
| Gene/Transgene symbol | Kcnab1 |
Information from provider
| Provider | Dirk Isbrandt |
| Provider affiliation | Center for Molecular Neurobiology, University Medical Center Hamburg |
| Genetic information | Targeted, general (non-tissue-specific) deletion of the Kvbeta1.1 (KCNAB1) gene in mice. |
| Phenotypic information | Kvbeta1.1 knockout mice are viable and fertile and do not display obvious phenotypic abnormalities. The loss of Kvbeta1.1 resulted in a reduced K+ current inactivation in hippocampal CA1 pyramidal neurons. Furthermore, in the mutant neurons, frequency-dependent spike broadening and the slow afterhyperpolarization (sAHP) were reduced. This suggests that Kvbeta1.1-dependent A-type K+ channels contribute to frequency-dependent spike broadening and may regulate the sAHP by controlling Ca2+ influx during action potentials. The Kvbeta1.1-deficient mice showed normal synaptic plasticity but were impaired in the learning of a water maze test and in the social transmission of food preference task, indicating that the Kvbeta1.1 subunit contributes to certain types of learning and memory. |
| Breeding history | Backcrossed to C57BL/6J for at least 15 generations. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Helmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH), Oberschleißheim, Germany |
Disease and phenotype information
MGI phenotypes (gene matching)
- abnormal spatial learning / MGI
- abnormal nervous system electrophysiology / MGI
- impaired social transmission of food preference / MGI
- enhanced long term potentiation / MGI
- abnormal impulse conducting system conduction / MGI
- abnormal afterhyperpolarization / MGI
- abnormal action potential / MGI
- mortality/aging / MGI
- abnormal inhibitory learning / MGI
Literature references
- Reduced K+ channel inactivation, spike broadening, and after-hyperpolarization in Kvbeta1.1-deficient mice with impaired learning.;Giese K P, Storm J F, Reuter D, Fedorov N B, Shao L R, Leicher T, Pongs O, Silva A J, ;1998;Learning & memory (Cold Spring Harbor, N.Y.);5;257-73; 10454353