Small-conductance, Ca2+-activated K+ channel SK3 generates age-related memory and LTP deficits

Small-conductance, Ca2+-activated K+ channel SK3 generates age-related memory and LTP deficits
复制标题

DOI:
10.1038/nn1101
复制
发表时间:
2003-09-01
影响因子:
25
通讯作者:
Spiess, J
Spiess, J
中科院分区:
医学1区
文献类型:
--
作者:
Blank, T;Nijholt, I;Spiess, J

文献摘要

被引文献

相似文献

认知缺陷是与衰老过程相关的最具破坏性的变化之一。与年龄相关的学习任务表现下降(1,2) 与海马体神经元信号处理的实质性变化相关(3-5)。在此,我们发现,老年小鼠海马中 SK3 型小电导 Ca2+ 激活的 K+ 通道(SK 通道)的表达升高有助于降低长时程增强 (LTP) 和受损的痕量恐惧条件反射,这是一项海马依赖性学习任务 (6,7)。
Cognitive deficits are among the most devastating changes associated with the aging process. Age-related decrement in performance on learning tasks(1,2) is correlated with substantial changes in neuronal signal processing in the hippocampus(3-5). Here we show that elevated expression of small-conductance Ca2+-activated K+ channels (SK channels) of the SK3 type in hippocampi of aged mice contributes to reduced long-term potentiation (LTP) and impaired trace fear conditioning, a hippocampus-dependent learning task(6,7).