Abstract
Amyloid beta (Aβ) induced neuronal death has been linked to memory loss, perhaps the most devastating symptom of Alzheimer’s disease (AD). Although Aβ-induced impairment of synaptic or intrinsic plasticity is known to occur before any cell death, the links between these neurophysiological changes and the loss of specific types of behavioral memory are not fully understood. Here we used a behaviorally and physiologically tractable animal model to investigate Aβ-induced memory loss and electrophysiological changes in the absence of neuronal death in a defined network underlying associative memory. We found similar behavioral but different neurophysiological effects for Aβ 25-35 and Aβ 1-42 in the feeding circuitry of the snail Lymnaea stagnalis. Importantly, we also established that both the behavioral and neuronal effects were dependent upon the animals having been classically conditioned prior to treatment, since Aβ application before training caused neither memory impairment nor underlying neuronal changes over a comparable period of time following treatment.
Highlights
Causing sufficient disturbance to result in learning and memory dysfunction[3,9,10,11,12]
We used this to our advantage and monitored the entry of systemically injected amyloid β (Aβ) into the buccal and cerebral ganglia, which contain all the circuitry involved in memory after food-reward conditioning[13]
We have identified a direct link between administration of Aβ and loss of consolidated long-term memory (LTM) in Lymnaea, a well-established and highly tractable model system for studying evolutionarily conserved cellular and molecular mechanisms of memory function and dysfunction[14]
Summary
Causing sufficient disturbance to result in learning and memory dysfunction[3,9,10,11,12] We believe that these early-stage disruptions are excellent targets for drug and clinical interference with AD and that more emphasis needs to be placed on pre-cell death studies. For this reason, we have examined the effects of Aβ treatment on the maintenance of established long-term memory (LTM) and underlying neuronal properties in the pond snail, Lymnaea stagnalis, with no signs of cell death in the neuronal circuitry for feeding that both acquires and stores the implicit memory trace after food-reward classical conditioning[13]. Aβ induced changes in behavior and neuronal properties only occurred when training preceded injection, suggesting a detrimental effect on memory maintenance or late/lingering consolidation rather than acquisition
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