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Alzheimer’s disease (AD) is the most prevalent form of neurodegenerative disorders characterized by neuritic plaques containing amyloidpeptide (A ) and neurofibrillary tangles. Evidence has been reported that A 1-42 plays an essential pathogenic role in decreased spine density, impairment of synaptic plasticity, and neuronal loss with disruption of memoryrelated synapse function, all associated with AD. Experimentally, A 1-42 oligomers perturb hippocampal long-term potentiation (LTP), an electrophysiological correlate of learning and memory. A was also reported to perturb synaptic glutamate (Glu)recycling by inhibiting excitatory-amino-acid-transporters. Elevated level of extracellular Glu leads to activation of perisynaptic receptors, including NR2B subunit containing NMDARs. These receptors were shown to induce impaired LTP and enhanced long-term depression and proapoptotic pathways, all central features of AD. In the present study, we investigated the role of Glu-recycling on A 1-42-induced LTP deficit in the CA1. We found that A -induced LTP damage, which was mimicked by the Glu-reuptake inhibitor TBOA, could be rescued by blocking the NR2B subunit of NMDA receptors. Furthermore, decreasing the level of extracellular Glu using a Glu scavenger also restores TBOA or A induces LTP damage. Overall, these results suggest that reducing ambient Glu in the brain can be protective against A -induced synaptic disruption.

Abeta(1-42) enhances neuronal excitability and disrupts synaptic plasticity by altering glutamate-recycling