How old mice get bright again

July 31, 2003

This release is also available in German.

All of us experience a successive decline in learning and memory capacities with ageing. In the course of their investigations of the neurophysiological basis of this decline, Thomas Blank, Ingrid Nijholt, Min-Jeong Kye, Jelena Radulovic, and Joachim Spiess from the Max Planck Institute for Experimental Medicine in Göttingen have obtained new insight into the mechanisms of age-related learning deficits in the mouse model. In experiments with mice, the Max Planck researchers were able to revert the observed age-related learning and memory deficits by down-regulation of calcium-activated potassium channels (SK3) located in the hippocampus, a brain region recognized to be important for learning and memory. The researchers published their results as a Brief Communication in the journal Nature Neuroscience.

In the study, young (4-6 months) and aged mice (22-24 months) had to learn that a defined tone was associated with a mild electric footshock serving as an aversive stimulus. If the tone was immediately followed by a footshock, young and aged mice remembered easily the association on the following day. They showed their memory by a so-called "freezing response" when exposed to the same tone used for training, but without application of a foot shock. This freezing, a naturally occurring defense behavior, is characterized by complete immobility of the mouse. The scientists then generated a more complex learning task by separating the tone from the shock by several seconds. As result of this change, the task now required specifically the hippocampus. Under these conditions, the aged mice were strongly impaired in comparison to the young mice. In agreement with the behavioral differences between aged and young mice, the scientists observed that "long-term potentiation" (LTP), an electrophysiological phenomenon indicating neuronal plasticity was lower in hippocampal brain tissue of aged mice when compared to LTP in hippocampus of young mice.

Moreover, using specific antibodies, the researchers found highly elevated levels of a calcium-activated potassium channel, the so-called SK3 channel, in the hippocampus of aged, but not of young mice. Most strikingly, when the researchers selectively downregulated SK3 channels in the hippocampus of aged mice, the impairment in learning and memory as well as in LTP was prevented. "Although it is anticipated that not a single gene, but rather a large number of genes is responsible for cognitive impairments induced by ageing, it seems promising from a therapeutic standpoint that interference with a single ion channel subtype can overcome certain age-dependent memory deficits," Joachim Spiess, Head of the Department of Molecular Neuroendocrinology at the Max Planck Institute of Experimental Medicine, says. "Our data suggest that increased SK3 channel expression in the hippocampus of aged mice represents a mechanism, which contributes to the age-dependent decline in learning, memory and LTP. 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 ageing", Thomas Blank adds.


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