Interaction of inhibition and triplets of excitatory spikes modulates the NMDA-R mediated synaptic plasticity in a computational model of spike timing dependent plasticity

Cutsuridis, Vassilis (2013) Interaction of inhibition and triplets of excitatory spikes modulates the NMDA-R mediated synaptic plasticity in a computational model of spike timing dependent plasticity. Hippocampus, 23 (1). pp. 75-86. ISSN 1050-9631

Full content URL: https://doi.org/10.1002/hipo.22057

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Abstract

Spike timing-dependent plasticity (STDP) experiments have
shown that a synapse is strengthened when a presynaptic spike precedes a
postsynaptic one and depressed vice versa. The canonical form of STDP
has been shown to have an asymmetric shape with the peak long-term
potentiation at 16 ms and the peak long-term depression at 25 ms. Experiments
in hippocampal cultures with more complex stimuli such as triplets
(one presynaptic spike combined with two postsynaptic spikes or one postsynaptic
spike with two presynaptic spikes) have shown that pre–post–pre
spike triplets result in no change in synaptic strength, whereas post–pre–
post spike triplets lead to significant potentiation. The sign and magnitude
of STDP have also been experimentally hypothesized to be modulated by
inhibition. Recently, a computational study showed that the asymmetrical
form of STDP in the CA1 pyramidal cell dendrite when two spikes interact
switches to a symmetrical one in the presence of inhibition under certain
conditions. In the present study, I investigate computationally how inhibition
modulates STDP in the CA1 pyramidal neuron dendrite when it is
driven by triplets. The model uses calcium as the postsynaptic signaling
agent for STDP and is shown to be consistent with the experimental triplet
observations in the absence of inhibition: simulated pre–post–pre spike
triplets result in no change in synaptic strength, whereas simulated post–
pre–post spike triplets lead to significant potentiation. When inhibition is
bounded by the onset and offset of the triplet stimulation, then the strength
of the synapse is decreased as the strength of inhibition increases.When inhibition
arrives either few milliseconds before or at the onset of the last
spike in the pre–post–pre triplet stimulation, then the synapse is potentiated.
Variability in the frequency of inhibition (50 vs. 100 Hz) produces no
change in synaptic strength. Finally, a 5% variation in model’s calcium parameters
(calcium thresholds) proves that the model’s performance is robust.

Keywords:computational model; STDP; calcium; NMDA; inhibition; hippocampus; CA1 pyramidal cell; triplets
Subjects:B Subjects allied to Medicine > B140 Neuroscience
G Mathematical and Computer Sciences > G730 Neural Computing
Divisions:College of Science > School of Computer Science
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ID Code:27725
Deposited On:03 Jul 2017 13:39

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