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+-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.
Blank
Thomas
T
Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D-37075 Goettingen, Germany.
Nijholt
Ingrid
I
Kye
Min-Jeong
MJ
Radulovic
Jelena
J
Spiess
Joachim
J
D000375:Aging / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D005786:Gene Expression Regulation / Q000502:physiology; D006624:Hippocampus / Q000378:metabolism; D017774:Long-Term Potentiation / Q000502:physiology*; D008569:Memory Disorders / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D015221:Potassium Channels / Q000096:biosynthesis* / Q000235:genetics; D024681:Potassium Channels, Calcium-Activated; D051640:Small-Conductance Calcium-Activated Potassium Channels
C496900:Kcnn3 protein, mouse; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; D051640:Small-Conductance Calcium-Activated Potassium Channels