Abstract
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.
Publication types
-
Comparative Study
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Aging / genetics
-
Aging / metabolism*
-
Animals
-
Gene Expression Regulation / physiology
-
Hippocampus / metabolism
-
Long-Term Potentiation / physiology*
-
Memory Disorders / genetics
-
Memory Disorders / metabolism*
-
Mice
-
Potassium Channels / biosynthesis*
-
Potassium Channels / genetics
-
Potassium Channels, Calcium-Activated*
-
Small-Conductance Calcium-Activated Potassium Channels
Substances
-
Kcnn3 protein, mouse
-
Potassium Channels
-
Potassium Channels, Calcium-Activated
-
Small-Conductance Calcium-Activated Potassium Channels