期刊
JOURNAL OF NEUROSCIENCE
卷 31, 期 45, 页码 16142-16156出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2520-11.2011
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资金
- Medical Research Council
- Engineering and Physical Sciences Research Council
- Biotechnology and Biological Sciences Research Council
- Human Frontier Science Program
- Marie Curie Excellence grant
- BBSRC [BB/H020284/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/H020284/1] Funding Source: researchfish
Long-term synaptic plasticity requires postsynaptic influx of Ca(2+) and is accompanied by changes in dendritic spine size. Unless Ca(2+) influx mechanisms and spine volume scale proportionally, changes in spine size will modify spine Ca(2+) concentrations during subsequent synaptic activation. We show that the relationship between Ca(2+) influx and spine volume is a fundamental determinant of synaptic stability. If Ca(2+) influx is undercompensated for increases in spine size, then strong synapses are stabilized and synaptic strength distributions have a single peak. In contrast, overcompensation of Ca(2+) influx leads to binary, persistent synaptic strengths with double-peaked distributions. Biophysical simulations predict that CA1 pyramidal neuron spines are undercompensating. This unifies experimental findings that weak synapses are more plastic than strong synapses, that synaptic strengths are unimodally distributed, and that potentiation saturates for a given stimulus strength. We conclude that structural plasticity provides a simple, local, and general mechanism that allows dendritic spines to foster both rapid memory formation and persistent memory storage.
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