Learning and memory impairments in Kvβ1.1-null mutants are rescued by environmental enrichment or ageing

Mice with a null mutation of the K(+) channel regulatory subunit K(v)beta1.1 have altered excitability in hippocampal neurons and are impaired in the social transmission of food preferences (STFP) task. It was previously unclear whether this impairment is related to learning and memory (L&M) deficits or to developmental abnormalities. In this study we show that rearing the K(v)beta1.1 mutants in an enriched environment rescues the impairment in the STFP task. Furthermore, we found that STFP performance was impaired in 12-month-old wild-type mice, but not in the K(v)beta1.1 mutants at this age, indicating that the K(v)beta1.1 mutants show an age-related rescue of the deficits observed in the young mutants. Ibotenic acid lesions of the hippocampus in the 12-month-old K(v)beta1.1 mutants caused an impairment in the STFP task. Our findings indicate that performance in the STFP task is age-dependent and involves the hippocampus. Furthermore, we have established that the impairments in the K(v)beta1.1 mutants are related to L&M and not to performance disabilities. Finally, we suggest that the loss of K(v)beta1.1 function is beneficial for L&M in middle age.