Spike-timing-dependent plasticity model for low-frequency pulse waveform

2019 ◽  
Vol 24 (4) ◽  
pp. 452-459
Author(s):  
Masaya Ohara ◽  
Minami Kaneko ◽  
Fumio Uchikoba ◽  
Ken Saito
Author(s):  
Niceto R. Luque ◽  
Jesús A. Garrido ◽  
Francisco Naveros ◽  
Richard R. Carrillo ◽  
Egidio D'Angelo ◽  
...  

2020 ◽  
Author(s):  
Yanis Inglebert ◽  
Johnatan Aljadeff ◽  
Nicolas Brunel ◽  
Dominique Debanne

AbstractLike many forms of long-term synaptic plasticity, spike-timing-dependent plasticity (STDP) depends on intracellular Ca2+ signaling for its induction. Yet, all in vitro studies devoted to STDP used abnormally high external Ca2+ concentration. We measured STDP at the CA3-CA1 hippocampal synapses under different extracellular Ca2+ concentrations and found that the sign, shape and magnitude of plasticity strongly depend on Ca2+. A pre-post protocol that results in robust LTP in high Ca2+, yielded only LTD or no plasticity in the physiological Ca2+ range. LTP could be restored by either increasing the number of post-synaptic spikes or increasing the pairing frequency. A calcium-based plasticity model in which depression and potentiation depend on post-synaptic Ca2+ transients was found to fit quantitatively all the data, provided NMDA receptor-mediated non-linearities were implemented. In conclusion, STDP rule is profoundly altered in physiological Ca2+ but specific activity regimes restore a classical STDP profile.


2006 ◽  
Vol 18 (10) ◽  
pp. 2414-2464 ◽  
Author(s):  
Peter A. Appleby ◽  
Terry Elliott

In earlier work we presented a stochastic model of spike-timing-dependent plasticity (STDP) in which STDP emerges only at the level of temporal or spatial synaptic ensembles. We derived the two-spike interaction function from this model and showed that it exhibits an STDP-like form. Here, we extend this work by examining the general n-spike interaction functions that may be derived from the model. A comparison between the two-spike interaction function and the higher-order interaction functions reveals profound differences. In particular, we show that the two-spike interaction function cannot support stable, competitive synaptic plasticity, such as that seen during neuronal development, without including modifications designed specifically to stabilize its behavior. In contrast, we show that all the higher-order interaction functions exhibit a fixed-point structure consistent with the presence of competitive synaptic dynamics. This difference originates in the unification of our proposed “switch” mechanism for synaptic plasticity, coupling synaptic depression and synaptic potentiation processes together. While three or more spikes are required to probe this coupling, two spikes can never do so. We conclude that this coupling is critical to the presence of competitive dynamics and that multispike interactions are therefore vital to understanding synaptic competition.


2015 ◽  
Vol 109 (6) ◽  
pp. 701-714 ◽  
Author(s):  
Carlo R. Laing ◽  
Ioannis G. Kevrekidis

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