Intrinsic stability of temporally shifted spike-timing dependent plasticity.

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...

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Main Authors: Baktash Babadi, L F Abbott
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2010-11-01
Series:PLoS Computational Biology
Online Access:http://europepmc.org/articles/PMC2973812?pdf=render
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spelling doaj-b5171a85cd5341af9f7bc016f01420522020-11-24T21:11:15ZengPublic Library of Science (PLoS)PLoS Computational Biology1553-734X1553-73582010-11-01611e100096110.1371/journal.pcbi.1000961Intrinsic stability of temporally shifted spike-timing dependent plasticity.Baktash BabadiL F AbbottSpike-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.http://europepmc.org/articles/PMC2973812?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Baktash Babadi
L F Abbott
spellingShingle Baktash Babadi
L F Abbott
Intrinsic stability of temporally shifted spike-timing dependent plasticity.
PLoS Computational Biology
author_facet Baktash Babadi
L F Abbott
author_sort Baktash Babadi
title Intrinsic stability of temporally shifted spike-timing dependent plasticity.
title_short Intrinsic stability of temporally shifted spike-timing dependent plasticity.
title_full Intrinsic stability of temporally shifted spike-timing dependent plasticity.
title_fullStr Intrinsic stability of temporally shifted spike-timing dependent plasticity.
title_full_unstemmed Intrinsic stability of temporally shifted spike-timing dependent plasticity.
title_sort intrinsic stability of temporally shifted spike-timing dependent plasticity.
publisher Public Library of Science (PLoS)
series PLoS Computational Biology
issn 1553-734X
1553-7358
publishDate 2010-11-01
description 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.
url http://europepmc.org/articles/PMC2973812?pdf=render
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