Learning and memory impairments in Kv beta 1.1-null mutants are rescued by environmental enrichment or ageing.
Mice with a null mutation of the K+ channel regulatory subunit Kv beta 1.1 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 Kv beta 1.1 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 Kv beta 1.1 mutants at this age, indicating that the Kv beta 1.1 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 Kv beta 1.1 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 Kv beta 1.1 mutants are related to L & M and not to performance disabilities. Finally, we suggest that the loss of Kv beta 1.1 function is beneficial for L & M in middle age.[1]References
- Learning and memory impairments in Kv beta 1.1-null mutants are rescued by environmental enrichment or ageing. Need, A.C., Irvine, E.E., Giese, K.P. Eur. J. Neurosci. (2003) [Pubmed]
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