EphB2 receptor forward signaling is needed for normal long-term memory formation in aged mice.

The molecular mechanisms underpinning age-related changes in the ability to form long-term memory need to be clarified. EphB2 receptors and their ephrin ligands are involved in key cellular functions such as neuronal morphogenesis and synaptic transmission believed to be involved in long-term memory formation. We were therefore interested to explore whether EphB2 is involved in the alterations in memory formation abilities observed in old age. Toward that end, we examined the ability to form long-term memory in mice that lack EphB2 (EphB2^-/-). A previous study has shown that the ability to form long-term conditioned taste aversion (CTA) memory in young EphB2^-/- mice remains intact. In the present study, we report that long-term CTA memory formation is improved in old wild-type mice but not in age-matched old EphB2^-/- mice. To further explore EphB2 mechanisms responsible for this difference in memory formation ability, we examined CTA memory in EphB2^lacZ/lacZ mice devoid of EphB2 forward signaling. We found that the ability to create CTA long-term memory is unaffected in young EphB2^lacZ/lacZ mice. However, the ability to form an increased long-term CTA memory shown in old wild-type mice is impaired in old EphB2^lacZ/lacZ mice. The inability to form enhanced CTA long-term memory in EphB2^-/- and EphB2^lacZ/lacZ old mice was not caused by differences in taste perception or ability to consume fluids. Thus, our observations show that the absence of EphB2 forward signaling in old mice impairs the ability to form enhanced long-term CTA memory and indicate that EphB2 forward signaling is needed for normal memory formation in aged mice.

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