| First Author | McGowan PO | Year | 2011 |
| Journal | Brain Res | Volume | 1383 |
| Pages | 187-95 | PubMed ID | 21354115 |
| Mgi Jnum | J:170703 | Mgi Id | MGI:4947165 |
| Doi | 10.1016/j.brainres.2011.02.054 | Citation | McGowan PO, et al. (2011) Impaired social recognition memory in recombination activating gene 1-deficient mice. Brain Res 1383:187-95 |
| abstractText | The recombination activating genes (RAGs) encode two enzymes that play key roles in the adaptive immune system. RAG1 and RAG2 mediate VDJ recombination, a process necessary for the maturation of B- and T-cells. Interestingly, RAG1 is also expressed in the brain, particularly in areas of high neural density such as the hippocampus, although its function is unknown. We tested evidence that RAG1 plays a role in brain function using a social recognition memory task, an assessment of the acquisition and retention of conspecific identity. In a first experiment, we found that RAG1-deficient mice show impaired social recognition memory compared to mice wildtype for the RAG1 allele. In a second experiment, by breeding to homogenize background genotype, we found that RAG1-deficient mice show impaired social recognition memory relative to heterozygous or RAG2-deficient littermates. Because RAG1 and RAG2 null mice are both immunodeficient, the results suggest that the memory impairment is not an indirect effect of immunological dysfunction. RAG1-deficient mice show normal habituation to non-socially derived odors and habituation to an open-field, indicating that the observed effect is not likely a result of a general deficit in habituation to novelty. These data trace the origin of the impairment in social recognition memory in RAG1-deficient mice to the RAG1 gene locus and implicate RAG1 in memory formation. |
