Effect of β-amyloid peptide on behavior and synaptic plasticity in terrestrial snail

A large body of evidence implicates beta-amyloid peptide (beta AP) and other derivatives of the evolutionarily highly conserved amyloid precursor protein (APP) in the pathogenesis of Alzheimer's disease. However. the functional relationship of APP and its proteolytic derivatives to synaptic plasticity is not well known. We demonstrate that 30 min exposure to the 25-35 fragment of beta AP do not markedly change the dynamics of synaptic responses in identified neurons of terrestrial snail while a significant decrease of long-term sensitization was observed after 180 min beta AP bath application. In the behavioral experiments, a significant reduction of sensitization. and decreased ability to develop food-aversion conditioning was observed after beta AP injection. Our results clearly demonstrate that the neurotoxic 25-35 fragment of beta AP may play a significant role in behavioral plasticity by chronically eliminating certain underlying forms of synaptic plasticity, The study also proposes a novel invertebrate model to Alzheimer's disease. (c) 2005 Elsevier Inc. All rights reserved.