期刊
EUROPEAN JOURNAL OF NEUROSCIENCE
卷 32, 期 2, 页码 231-240出版社
WILEY
DOI: 10.1111/j.1460-9568.2010.07345.x
关键词
calcium; energy; mitochondria; synapse; transport
资金
- MRC (UK)
- MRC [G0802377] Funding Source: UKRI
Neuronal postsynaptic currents consume most of the brain's energy supply. Delineating how neurons control the distribution, morphology and function of the energy-producing mitochondria that fuel synaptic communication is therefore important for our understanding of nervous system function and pathology. Here we review recent insights into the molecular mechanisms that control activity-dependent regulation of mitochondrial trafficking, morphology and activity at excitatory synapses. We also consider some implications of this regulation for synaptic function and plasticity and discuss how this may contribute to synaptic dysfunction and signalling in neurological disease, with a focus on Alzheimer's disease.
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