Researchers Overcome Age-Related Memory Deficits in Mice

If the tone was immediately followed by the foot shock, young and aged mice remembered the association the next day. They showed their memory by a "freezing response” when exposed to the tone without the foot shock. Then the researchers made the learning task more complex by separating the tone from the shock by several seconds. The task now specifically required the hippocampus. The aged mice were shown to be strongly impaired in this exercise, compared to the young mice. The researchers observed that long-term potentiation (LTP), which indicates neuronal plasticity, was lower in hippocampal brain tissue of aged mice.

Using specific antibodies, the researchers found highly elevated levels of a calcium-activated potassium channel, SK3, in the hippocampus of aged mice but not of young mice. When the SK3 channels were selectively down-regulated in the hippocampus of aged mice, the impairment in learning, memory, and LTP was prevented.

"Our data suggest that increased SK3 channel expression in the hippocampus of aged mice represents a mechanism that contributes to the age-dependent decline in learning, memory, and LTP,” observed Thomas Blank, of the Max Planck Institute for Experimental Medicine (Gottingen, Germany; www.maxplanck.de). An intervention that selectively reduces the function of SK3 channels may therefore be a novel mechanistic approach for pharmacological treatments that might relieve or even prevent memory deficits associated with aging.”




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