Intrinsic Stability of Temporally Shifted Spike-Timing Dependent Plasticity

被引:49
作者
Babadi, Baktash [1 ]
Abbott, L. F. [1 ,2 ]
机构
[1] Columbia Univ, Dept Neurosci, Ctr Theoret Neurosci, New York, NY 10027 USA
[2] Columbia Univ Coll Phys & Surg, Dept Physiol & Cellular Biophys, New York, NY 10032 USA
关键词
ASYMMETRIC HEBBIAN PLASTICITY; CA1 PYRAMIDAL NEURONS; SYNAPTIC PLASTICITY; SIMPLE-MODEL; DENDRITES; LOCATION; INPUT; NMDA; VARIABILITY; INTEGRATION;
D O I
10.1371/journal.pcbi.1000961
中图分类号
Q5 [生物化学];
学科分类号
070307 [化学生物学];
摘要
Spike-timing dependent plasticity (STDP), a widespread synaptic modification mechanism, is sensitive to correlations between presynaptic spike trains and it generates competition among synapses. However, STDP has an inherent instability because strong synapses are more likely to be strengthened than weak ones, causing them to grow in strength until some biophysical limit is reached. Through simulations and analytic calculations, we show that a small temporal shift in the STDP window that causes synchronous, or nearly synchronous, pre- and postsynaptic action potentials to induce long-term depression can stabilize synaptic strengths. Shifted STDP also stabilizes the postsynaptic firing rate and can implement both Hebbian and anti-Hebbian forms of competitive synaptic plasticity. Interestingly, the overall level of inhibition determines whether plasticity is Hebbian or anti-Hebbian. Even a random symmetric jitter of a few milliseconds in the STDP window can stabilize synaptic strengths while retaining these features. The same results hold for a shifted version of the more recent "triplet" model of STDP. Our results indicate that the detailed shape of the STDP window function near the transition from depression to potentiation is of the utmost importance in determining the consequences of STDP, suggesting that this region warrants further experimental study.
引用
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页数:14
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