期刊
SCIENCE
卷 321, 期 5896, 页码 1686-1689出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1162844
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资金
- Deutsche Forschungsgemeinschaft [SFB 596, GA 654/1-1, HO 2156/2-1]
- Helmholtz Gemeinschaft.
The neurodegeneration observed in Alzheimer's disease has been associated with synaptic dismantling and progressive decrease in neuronal activity. We tested this hypothesis in vivo by using two- photon Ca(2+) imaging in a mouse model of Alzheimer's disease. Although a decrease in neuronal activity was seen in 29% of layer 2/3 cortical neurons, 21% of neurons displayed an unexpected increase in the frequency of spontaneous Ca(2+) transients. These hyperactive neurons were found exclusively near the plaques of amyloid beta-depositing mice. The hyperactivity appeared to be due to a relative decrease in synaptic inhibition. Thus, we suggest that a redistribution of synaptic drive between silent and hyperactive neurons, rather than an overall decrease in synaptic activity, provides a mechanism for the disturbed cortical function in Alzheimer's disease.
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