Mice with a null mutation of the K+ channel regulatory subunit Kvβ1.1 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 Kvβ1.1 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 Kvβ1.1 mutants at this age, indicating that the Kvβ1.1 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 Kvβ1.1 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 Kvβ1.1 mutants are related to L & M and not to performance disabilities. Finally, we suggest that the loss of Kvβ1.1 function is beneficial for L & M in middle age.