Need Anna C, Irvine Elaine E, Giese K Peter
Wolfson Institute for Biomedical Research, University College London, Gower Street, London, WC1E 6BT, UK.
Eur J Neurosci. 2003 Sep;18(6):1640-4. doi: 10.1046/j.1460-9568.2003.02889.x.
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.
钾离子通道调节亚基Kvβ1.1基因发生无效突变的小鼠，其海马神经元的兴奋性发生改变，并且在食物偏好的社会传递（STFP）任务中表现受损。此前尚不清楚这种损害是与学习和记忆（L&M）缺陷有关，还是与发育异常有关。在本研究中，我们发现，在丰富环境中饲养Kvβ1.1突变体可挽救其在STFP任务中的损害。此外，我们发现12月龄野生型小鼠在STFP任务中的表现受损，但该年龄的Kvβ1.1突变体则未受损，这表明Kvβ1.1突变体在年龄增长过程中出现了对年轻突变体中观察到的缺陷的挽救现象。12月龄Kvβ1.1突变体的海马经鹅膏蕈氨酸损伤后，其在STFP任务中出现损害。我们的研究结果表明，STFP任务中的表现具有年龄依赖性，并且涉及海马。此外，我们已经确定，Kvβ1.1突变体中的损害与学习和记忆有关，而非与行为能力缺陷有关。最后，我们认为Kvβ1.1功能的丧失对中年时期的学习和记忆有益。
