Astrocyte-originated ATP protects Aβ 1-42-induced impairment of synaptic plasticity

Eun Sun Jung, Kyongman An, Hyun Seok Hong, Joung Hun Kim, Inhee Mook-Jung

Research output: Contribution to journalArticlepeer-review

Abstract

Activated microglia and reactive astrocytes are commonly found in and around the senile plaque, which is the central pathological hallmark of Alzheimer's disease. Astrocytes respond to neuronal activity through the release of gliotransmitters such as glutamate, D-serine, and ATP. However, it is largely unknown whether and how gliotransmitters affect neuronal functions. In this study, we explored the effect of a gliotransmitter, ATP, on neurons damaged byβ-amyloid peptide (Aβ). We found that Aβ 1-42 (Aβ42) increased the release of ATP in cultures of primary astrocytes and U373 astrocyte cell line. We also found that exogenous ATP protected Aβ42-mediated reduction in synaptic molecules, such as NMDA receptor 2A and PSD-95, through P2 purinergic receptors and prevented Aβ42-induced spine reduction in cultured primary hippocampal neurons. Moreover, ATP prevented Aβ42-induced impairment of long-term potentiation in acute hippocampal slices. Our findings suggest that Aβ-induced release of gliotransmitter ATP plays a protective role against Aβ42-mediated disruption of synaptic plasticity.

Original languageEnglish (US)
Pages (from-to)3081-3087
Number of pages7
JournalJournal of Neuroscience
Volume32
Issue number9
DOIs
StatePublished - Feb 29 2012
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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