Contribution of Individual Spikes in Burst-Induced Long-Term Synaptic Modification

Froemke, Robert C.; Tsay, Ishan A.; Raad, Mohamad; Long, John D.; Dan, Yang

doi:10.1152/jn.00910.2005

Cited by 192 publications

(331 citation statements)

References 55 publications

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“…If we apply the same STDP model not only to RGC-TN synapses but also to TN-TN synapses, all of the TN-TN synapses may be potentiated by the repetitive exposure of the retina to the fast-moving light bar. This corresponds to the situation in which burst firings in both pre-neurons and postneurons lead to potentiation, regardless of the order of the firings in pre-neurons and post-neurons (Froemke et al, 2006;Urakubo et al, 2008). In this case with STDP at TN-TN synapses, stronger early transient feedforward signals and the decrease in the transition threshold of feedback excitation due to the potentiation of all TN-TN synapses are similarly likely to lead to the development of direction selectivity.…”

Section: Stdp In Tn-tn Synapsesmentioning

confidence: 93%

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Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

Honda¹,

Urakubo²,

Tanaka³

et al. 2011

J. Neurosci.

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The development of direction selectivity in the visual system depends on visual experience. In the developing Xenopus retinotectal system, tectal neurons (TNs) become direction selective through spike timing-dependent plasticity (STDP) after repetitive retinal exposure to a moving bar in a specific direction. We investigated the mechanism responsible for the development of direction selectivity in the Xenopus retinotectal system using a neural circuit model with STDP. In this retinotectal circuit model, a moving bar stimulated the retinal ganglion cells (RGCs), which provided feedforward excitation to the TNs and interneurons (INs). The INs provided delayed feedforward inhibition to the TNs. The TNs also received feedback excitation from neighboring TNs. As a synaptic learning rule, a molecular STDP model was used for synapses between the RGCs and TNs. The retinotectal circuit model reproduced experimentally observed features of the development of direction selectivity, such as increase in input to the TN. The peak of feedforward excitation from RGCs to TNs shifted earlier as a result of STDP. Together with the delayed feedforward inhibition, a stronger earlier transient feedforward signal was generated, which exceeded the threshold of the feedback excitation from the neighboring TNs and resulted in amplification of input to the TN. The suppression of the delayed feedforward inhibition resulted in the development of orientation selectivity rather than direction selectivity, indicating the pivotal role of the delayed feedforward inhibition in direction selectivity. We propose a mechanism for the development of direction selectivity involving a delayed feedforward inhibition with STDP and the amplification of feedback excitation.

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Section: Stdp In Tn-tn Synapsesmentioning

confidence: 93%

“…1B; supplemental Fig. 7, available at www.jneurosci.org as supplemental material) (Froemke and Dan, 2002;Froemke et al, 2006;Ur-akubo et al, 2008). This simple STDP model can be used to test the development of direction selectivity.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

Honda¹,

Urakubo²,

Tanaka³

et al. 2011

J. Neurosci.

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“…Supplementary Figs. 4,5), we measured synaptic strength as the first 2 ms of the EPSP slope 31 . A 'burst' of spikes was defined as two or more spikes with an inter-spike interval of <10 ms.…”

Section: Methodsmentioning

confidence: 99%

A synaptic memory trace for cortical receptive field plasticity

Froemke

Merzenich

Schreiner

2007

Nature

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568

580

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A synaptic memory trace for cortical receptive field plasticity. Neuromodulation is required for cortical plasticity, but it is uncertain how subcortical neuromodulatory systems, such as the cholinergic nucleus basalis ( A major subcortical nucleus critical for receptive field plasticity is NB, the main source of cortical acetylcholine (ACh) 4,9,[14][15][16][17][19][20][21] . How are neuromodulators such as ACh involved in plasticity, and what circuit elements do they act upon? One possibility is that neuromodulation creates a cellular tag or memory trace for synaptic events that occurred in conjunction with neuromodulator release. However, the effects of ACh on cortical

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“…For a given postsynaptic spike, all the synapses that fire before the spike are potentiated (to a degree which depends on their time difference, t post -t pre ), whereas all the synapses firing after the spike are depressed (see also Bi and Wang 2002;Froemke and Dan 2002;Froemke et al 2006;Sjöström et al 2001).…”

Section: Modeling Different Stdp Rulesmentioning

confidence: 99%

Spike-Timing–Dependent Synaptic Plasticity and Synaptic Democracy in Dendrites

Gidon¹,

Segev²

2009

Journal of Neurophysiology

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Gidon A, Segev I. Spike-timing-dependent synaptic plasticity and synaptic democracy in dendrites. J Neurophysiol 101: 3226 -3234, 2009. First published April 8, 2009 doi:10.1152/jn.91349.2008. We explored in a computational study the effect of dendrites on excitatory synapses undergoing spike-timing-dependent plasticity (STDP), using both cylindrical dendritic models and reconstructed dendritic trees. We show that even if the initial strength, g peak , of distal synapses is augmented in a location independent manner, the efficacy of distal synapses diminishes following STDP and proximal synapses would eventually dominate. Indeed, proximal synapses always win over distal synapses following linear STDP rule, independent of the initial synaptic strength distribution in the dendritic tree. This effect is more pronounced as the dendritic cable length increases but it does not depend on the dendritic branching structure. Adding a small multiplicative component to the linear STDP rule, whereby already strong synapses tend to be less potentiated than depressed (and vice versa for weak synapses) did partially "save" distal synapses from "dying out." Another successful strategy for balancing the efficacy of distal and proximal synapses following STDP is to increase the upper bound for the synaptic conductance (g max ) with distance from the soma. We conclude by discussing an experiment for assessing which of these possible strategies might actually operate in dendrites. Hebb (1949) introduced his famous postulate for the mechanism that may underlie activity-dependent synaptic plasticity 60 years ago. In the last 10 years, experimental studies have begun to unravel the operation of such a mechanism and it has been shown that, in many neuron types, the precise timing of the pre-versus the postsynaptic spikes play a critical role in determining the efficacy of the synaptic connection between neurons [spike-timing-dependent plasticity (STDP)] (Bell et al. 1997;Bi and Poo 1998;Debanne et al. 1998;Markram et al. 1997;Zhang et al. 1998; reviews by Poo 2006 andNelson 2000). This specific type of synaptic plasticity operates within a time window of tens of milliseconds, and its direction and magnitude are critically determined by the temporal order of the pre-versus the postsynaptic spike. If a synapse is active before the postsynaptic neuron fired a spike (pre before post), the efficacy of this synapse is enhanced; the synapse is weakened for the reverse temporal order (post before pre). Outside of the critical temporal window for STDP, the efficacy of the synapse remains unchanged.These experimental studies were followed by theoretical efforts to understand the biophysical foundation of STDP (Shouval et al. 2002) One interesting question regarding STDP is its role in selectively "configuring" the synaptic efficacy at different dendritic locations. Because neurons are inhomogeneous in their morphology and membrane properties, synaptic contacts at different locations on the dendrite would be influenced by different specific dendr...

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Contribution of Individual Spikes in Burst-Induced Long-Term Synaptic Modification

Cited by 192 publications

References 55 publications

Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

A synaptic memory trace for cortical receptive field plasticity

Spike-Timing–Dependent Synaptic Plasticity and Synaptic Democracy in Dendrites

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