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- Title
Astrocyte-Originated ATP Protects A&BGR;<sub>1-42</sub>-Induced Impairment of Synaptic Plasticity.
- Authors
Eun Sun Jung; Kyongman An; Hyun Seok Hong; Joung-Hun Kim; Inhee Mook-Jung
- 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 by&BGR;-amyloid peptide (A&BGR;). We found that A&BGR;1-42 (A&BGR;42) increased the release of ATP in cultures of primary astrocytes and U373 astrocyte cell line. We also found that exogenous ATP protected A&BGR;42-mediated reduction in synaptic molecules, such as NMDA receptor 2A and PSD-95, through P2 purinergic receptors and prevented A&BGR;42-induced spine reduction in cultured primary hippocampal neurons. Moreover, ATP prevented A&BGR;42-induced impairment of long-term potentiation in acute hippocampal slices. Our findings suggest that A&BGR;-induced release of gliotransmitter ATP plays a protective role against A&BGR;42-mediated disruption of synaptic plasticity.
- Subjects
ADENOSINE triphosphate; ASTROCYTES; NEUROPLASTICITY; NEUROLOGICAL disorders; PATHOLOGY; ALZHEIMER'S disease; GLUTAMIC acid; NEUROTRANSMITTERS
- Publication
Journal of Neuroscience, 2012, Vol 32, Issue 9, p3081
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.6357-11.2012