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

Cognitive deficits are among the most devastating changes associated with the aging process. Age-related decrement in performance on learning tasks is correlated with substantial changes in neuronal signal processing in the hippocampus. Here we show that elevated expression of small-conductance Ca2+...

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Bibliographic Details
Published inNature neuroscience Vol. 6; no. 9; pp. 911 - 912
Main Authors Blank, Thomas, Nijholt, Ingrid, Kye, Min-Jeong, Radulovic, Jelena, Spiess, Joachim
Format Journal Article
LanguageEnglish
Published United States Nature Publishing Group 01.09.2003
Subjects
Aging - genetics
Aging - metabolism
Animals
Calcium ions
Gene Expression Regulation - physiology
Hippocampus - metabolism
Long-term potentiation
Long-Term Potentiation - physiology
Memory Disorders - genetics
Memory Disorders - metabolism
Mice
Physiological aspects
Potassium channels
Potassium Channels - biosynthesis
Potassium Channels - genetics
Potassium Channels, Calcium-Activated
Small-Conductance Calcium-Activated Potassium Channels
Germany
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Summary:Cognitive deficits are among the most devastating changes associated with the aging process. Age-related decrement in performance on learning tasks is correlated with substantial changes in neuronal signal processing in the hippocampus. 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.
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ISSN:1097-6256
1546-1726
DOI:10.1038/nn1101