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

Nat Neurosci. 2003 Sep;6(9):911-2. doi: 10.1038/nn1101.


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


  • Kcnn3 protein, mouse
  • Potassium Channels
  • Potassium Channels, Calcium-Activated
  • Small-Conductance Calcium-Activated Potassium Channels