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Academic Commons Search Resultsen-usStability and Competition in Multi-spike Models of Spike-Timing Dependent Plasticity
http://academiccommons.columbia.edu/catalog/ac:197941
Babadi, Baktash; Abbott, Larryhttp://dx.doi.org/10.7916/D8930T51Wed, 27 Apr 2016 00:00:00 +0000Spike-timing dependent plasticity (STDP) is a widespread plasticity mechanism in the nervous system. The simplest description of STDP only takes into account pairs of pre- and postsynaptic spikes, with potentiation of the synapse when a presynaptic spike precedes a postsynaptic spike and depression otherwise. In light of experiments that explored a variety of spike patterns, the pair-based STDP model has been augmented to account for multiple pre- and postsynaptic spike interactions. As a result, a number of different “multi-spike” STDP models have been proposed based on different experimental observations. The behavior of these models at the population level is crucial for understanding mechanisms of learning and memory. The challenging balance between the stability of a population of synapses and their competitive modification is well studied for pair-based models, but it has not yet been fully analyzed for multi-spike models. Here, we address this issue through numerical simulations of an integrate-and-fire model neuron with excitatory synapses subject to STDP described by three different proposed multi-spike models. We also analytically calculate average synaptic changes and fluctuations about these averages. Our results indicate that the different multi-spike models behave quite differently at the population level. Although each model can produce synaptic competition in certain parameter regions, none of them induces synaptic competition with its originally fitted parameters. The dichotomy between synaptic stability and Hebbian competition, which is well characterized for pair-based STDP models, persists in multi-spike models. However, anti-Hebbian competition can coexist with synaptic stability in some models. We propose that the collective behavior of synaptic plasticity models at the population level should be used as an additional guideline in applying phenomenological models based on observations of single synapses.Neurosciences, Biology, Biochemistry, Neuroplasticity, Synapses, Neurosciences--Researchbb2280, lfa2103NeuroscienceArticlesPairwise Analysis Can Account for Network Structures Arising from Spike-Timing Dependent Plasticity
http://academiccommons.columbia.edu/catalog/ac:162971
Babadi, Baktash; Abbott, Larryhttp://hdl.handle.net/10022/AC:P:20970Wed, 10 Jul 2013 00:00:00 +0000Spike timing-dependent plasticity (STDP) modifies synaptic strengths based on timing information available locally at each synapse. Despite this, it induces global structures within a recurrently connected network. We study such structures both through simulations and by analyzing the effects of STDP on pair-wise interactions of neurons. We show how conventional STDP acts as a loop-eliminating mechanism and organizes neurons into in- and out-hubs. Loop-elimination increases when depression dominates and turns into loop-generation when potentiation dominates. STDP with a shifted temporal window such that coincident spikes cause depression enhances recurrent connections and functions as a strict buffering mechanism that maintains a roughly constant average firing rate. STDP with the opposite temporal shift functions as a loop eliminator at low rates and as a potent loop generator at higher rates. In general, studying pairwise interactions of neurons provides important insights about the structures that STDP can produce in large networks.Biology, Systematic biology, Neurosciencesbb2280, lfa2103NeuroscienceArticlesNetwork Structures Arising from Spike-Timing Dependent Plasticity
http://academiccommons.columbia.edu/catalog/ac:137854
Babadi, Baktashhttp://hdl.handle.net/10022/AC:P:11016Mon, 29 Aug 2011 00:00:00 +0000Spike-timing dependent plasticity (STDP), a widespread synaptic modification mechanism, is sensitive to correlations between presynaptic spike trains, and organizes neural circuits in functionally useful ways. In this dissertation, I study the structures arising from STDP in a population of synapses with an emphasis on the interplay between synaptic stability and Hebbian competition, explained in Chapter 1. Starting from the simplest description of STDP which relates synaptic modification to the intervals between pairs of pre- and postsynaptic spikes, I show in Chapter 2 that stability and Hebbian competition are incompatible in this class of ``pair-based'' STDP models, either when hard bounds or soft bounds are imposed to the synapses. In chapter 3, I propose an alternative biophysically inspired method for imposing bounds to synapses, i.e. introducing a small temporal shift in the STDP window. Shifted STDP overcomes the incompatibility of synaptic stability and competition and can implement both Hebbian and anti-Hebbian forms of competitive plasticity. In light of experiments the explored a variety of spike patterns, STDP models have been augmented to account for interactions between multiple pre- and postsynaptic action potentials. In chapter 4, I study the stability/competition interplay in three different proposed multi-spike models of STDP. I show that the ``triplet model'' leads to a partially steady-state distribution of synaptic weights and induces Hebbian competition. The ``suppression model'' develops a stable distribution of weights when the average weight is high and shows predominantly anti-Hebbian competition. The "NMDAR-based" model can lead to either stable or partially stable synaptic weight distribution and exhibits both Hebbian and anti-Hebbian competition, depending on the parameters. I conclude that multi-spike STDP models can produce radically different effects at the population level depending on how they implement multi-spike interactions. Finally in chapter 5, I focus on the types of global structures that arise from STDP in a recurrent network. By analyzing pairwise interactions of neurons through STDP and also numerical simulations of a large network, I show that conventional pair-based STDP functions as a loop-eliminating mechanism in a network of spiking neurons and organizes neurons into in- and out-hubs. Loop-elimination increases when depression dominates and decreases when potentiation dominates. STDP with dominant depression implements a buffering mechanism for network firing rates, and shifted STDP can generate recurrent connections in a network, and also functions as a homeostatic mechanism that maintains a roughly constant average value of the synaptic strengths. In conclusion, studying pairwise interactions of neurons through STDP provides a number of important insights about the structures that arise from this plasticity rule in large networks. This approach can be extended to networks with more complex STDP models and more structured external input.Nanoscience, Biophysicsbb2280Neurobiology and Behavior, Physiology and Cellular Biophysics, NeuroscienceDissertations