A Calcium-Based Simple Model of Multiple Spike Interactions in Spike-Timing-Dependent Plasticity

2013 ◽  
Vol 25 (7) ◽  
pp. 1853-1869 ◽  
Author(s):  
Takumi Uramoto ◽  
Hiroyuki Torikai
Keyword(s):  
Synaptic Weight ◽  
Spike Timing ◽  
State Variables ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Synaptic Modification ◽  
Proposed Model ◽  
Layer 2 ◽  
Visual Cortical ◽  
Cortical Slices

Spike-timing-dependent plasticity (STDP) is a form of synaptic modification that depends on the relative timings of presynaptic and postsynaptic spikes. In this letter, we proposed a calcium-based simple STDP model, described by an ordinary differential equation having only three state variables: one represents the density of intracellular calcium, one represents a fraction of open state NMDARs, and one represents the synaptic weight. We shown that in spite of its simplicity, the model can reproduce the properties of the plasticity that have been experimentally measured in various brain areas (e.g., layer 2/3 and 5 visual cortical slices, hippocampal cultures, and layer 2/3 somatosensory cortical slices) with respect to various patterns of presynaptic and postsynaptic spikes. In addition, comparisons with other STDP models are made, and the significance and advantages of the proposed model are discussed.

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

2006 ◽  
Vol 95 (3) ◽  
pp. 1620-1629 ◽  
Author(s):  
Robert C. Froemke ◽  
Ishan A. Tsay ◽  
Mohamad Raad ◽  
John D. Long ◽  
Yang Dan
Keyword(s):  
High Frequency ◽  
Spike Timing ◽  
Relative Timing ◽  
Short Term ◽  
Burst Frequency ◽  
Synaptic Modification ◽  
Visual Cortical ◽  
Cortical Slices ◽  
Dependent Interaction

Long-term synaptic modification depends on the relative timing of individual pre- and postsynaptic spikes, but the rules governing the effects of multispike bursts remain to be fully understood. In particular, some studies suggest that the spike timing dependence of synaptic modification breaks down with high-frequency bursts. In this study, we characterized the effects of pre- and postsynaptic bursts on long-term modification of layer 2/3 synapses in visual cortical slices from young rats. We found that, while pairing-induced synaptic modification depends on the burst frequency, this dependence can be explained in terms of the timing of individual pre- and postsynaptic spikes. Later spikes in each burst are less effective in synaptic modification, but spike efficacy is regulated differently in pre- and postsynaptic bursts. Presynaptically, spike efficacy is progressively weakened, in parallel with short-term synaptic depression. Postsynaptically, spike efficacy is suppressed to a lesser extent, and it depends on postsynaptic potassium channel activation. Such timing-dependent interaction among multiple spikes can account for synaptic modifications induced by a variety of spike trains, including the frequency-dependent transition from depression to potentiation induced by a postsynaptic burst preceding a presynaptic burst.

Identification of Stable Spike-Timing-Dependent Plasticity from Spiking Activity with Generalized Multilinear Modeling

2016 ◽  
Vol 28 (11) ◽  
pp. 2320-2351 ◽  
Author(s):  
Brian S. Robinson ◽  
Theodore W. Berger ◽  
Dong Song
Keyword(s):  
Learning And Memory ◽  
Spike Timing ◽  
System Stability ◽  
Optimization Approach ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Synaptic Modification ◽  
Spiking Neuron Model ◽  
Underlying Mechanisms ◽  
Spiking Activity

Characterization of long-term activity-dependent plasticity from behaviorally driven spiking activity is important for understanding the underlying mechanisms of learning and memory. In this letter, we present a computational framework for quantifying spike-timing-dependent plasticity (STDP) during behavior by identifying a functional plasticity rule solely from spiking activity. First, we formulate a flexible point-process spiking neuron model structure with STDP, which includes functions that characterize the stationary and plastic properties of the neuron. The STDP model includes a novel function for prolonged plasticity induction, as well as a more typical function for synaptic weight change based on the relative timing of input-output spike pairs. Consideration for system stability is incorporated with weight-dependent synaptic modification. Next, we formalize an estimation technique using a generalized multilinear model (GMLM) structure with basis function expansion. The weight-dependent synaptic modification adds a nonlinearity to the model, which is addressed with an iterative unconstrained optimization approach. Finally, we demonstrate successful model estimation on simulated spiking data and show that all model functions can be estimated accurately with this method across a variety of simulation parameters, such as number of inputs, output firing rate, input firing type, and simulation time. Since this approach requires only naturally generated spikes, it can be readily applied to behaving animal studies to characterize the underlying mechanisms of learning and memory.

Inhibition of the slow afterhyperpolarization restores the classical spike timing-dependent plasticity rule obeyed in layer 2/3 pyramidal cells of the prefrontal cortex

2012 ◽  
Vol 107 (1) ◽  
pp. 205-215 ◽  
Author(s):  
Aleksey V. Zaitsev ◽  
Roger Anwyl
Keyword(s):  
Prefrontal Cortex ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Layer 2 ◽  
Stdp Rule ◽  
Stimulation Of

The induction of long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic currents was investigated in proximal synapses of layer 2/3 pyramidal cells of the rat medial prefrontal cortex. The spike timing-dependent plasticity (STDP) induction protocol of negative timing, with postsynaptic leading presynaptic stimulation of action potentials (APs), induced LTD as expected from the classical STDP rule. However, the positive STDP protocol of presynaptic leading postsynaptic stimulation of APs predominantly induced a presynaptically expressed LTD rather than the expected postsynaptically expressed LTP. Thus the induction of plasticity in layer 2/3 pyramidal cells does not obey the classical STDP rule for positive timing. This unusual STDP switched to a classical timing rule if the slow Ca2+-dependent, K+-mediated afterhyperpolarization (sAHP) was inhibited by the selective blocker N-trityl-3-pyridinemethanamine (UCL2077), by the β-adrenergic receptor agonist isoproterenol, or by the cholinergic agonist carbachol. Thus we demonstrate that neuromodulators can affect synaptic plasticity by inhibition of the sAHP. These findings shed light on a fundamental question in the field of memory research regarding how environmental and behavioral stimuli influence LTP, thereby contributing to the modulation of memory.

Soft-Reward Based Reinforcement Learning by Spiking Neural Networks

2011 ◽  
Vol 219-220 ◽  
pp. 770-773
Author(s):  
Wei Ya Shi
Keyword(s):  
Neural Networks ◽  
Reinforcement Learning ◽  
Synaptic Weight ◽  
Spike Timing ◽  
Benchmark Dataset ◽  
Spiking Neural Networks ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Winner Take All ◽  
Take All

In this paper, we propose algorithm based reinforcement learning for spiking neural networks. The algorithm simulates biological adaptability and uses the soft-reward from environment to modulate the synaptic weight, which combines spike-timing-dependent plasticity (STDP), winner-take-all mechanism. The algorithm is tested to classify a number of standard benchmark dataset. The obtained results show the effectiveness of the proposed algorithm.

scholarly journals BIOPHYSICAL AND PHENOMENOLOGICAL MODELS OF MULTIPLE SPIKE INTERACTIONS IN SPIKE-TIMING DEPENDENT PLASTICITY

2006 ◽  
Vol 16 (02) ◽  
pp. 79-97 ◽  
Author(s):  
MATHILDE BADOUAL ◽  
QUAN ZOU ◽  
ANDREW P. DAVISON ◽  
MICHAEL RUDOLPH ◽  
THIERRY BAL ◽  
...  
Keyword(s):  
Numerical Simulation ◽  
Phenomenological Model ◽  
Analytical Investigation ◽  
Spike Timing ◽  
Biophysical Model ◽  
Spike Timing Dependent Plasticity ◽  
Frequency Dependency ◽  
Dependent Plasticity ◽  
Synaptic Modification ◽  
The Impact

Spike-timing dependent plasticity (STDP) is a form of associative synaptic modification which depends on the respective timing of pre- and post-synaptic spikes. The biophysical mechanisms underlying this form of plasticity are currently not known. We present here a biophysical model which captures the characteristics of STDP, such as its frequency dependency, and the effects of spike pair or spike triplet interactions. We also make links with other well-known plasticity rules. A simplified phenomenological model is also derived, which should be useful for fast numerical simulation and analytical investigation of the impact of STDP at the network level.

scholarly journals Muscarinic modulation of spike-timing dependent plasticity at recurrent layer 2/3 synapses in mouse auditory cortex

2019 ◽  
Author(s):  
Deepti Rao ◽  
Megan B. Kratz ◽  
Paul B. Manis
Keyword(s):  
Auditory Cortex ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Receptor Modulation ◽  
Intracortical Circuits ◽  
Layer 2

AbstractCholinergic systems contribute to the refinement of auditory cortical receptive fields by activating muscarinic acetylcholine receptors (mAChRs). However, the specific cellular and synaptic mechanisms underlying acetylcholine’s effects on cortical circuits are not fully understood. In this study, we investigate the effects of muscarinic receptor modulation on spike-timing dependent plasticity (STDP) at synapses onto layer 2/3 pyramidal neurons in mouse auditory cortex (AC). Synapses onto layer 2/3 pyramidal neurons exhibit a STDP rule for pairing of postsynaptic spike bursts with single presynaptic stimuli. Pre-before-post pairing at +10 ms results in a timing-dependent long-term potentiation (tLTP), whereas pre-before-post pairing at +50 ms intervals, and post-before-pre pairing at -10 to -20 ms produce a timing-dependent long-term depression. We also characterize how mAChR activation affects plasticity at these synapses, focusing on the induction of tLTP. During pre-before-post pairing at +10 ms, mAChR activation by either carbachol or oxotremorine-M suppresses tLTP. mAChR activation also reduces the NMDA-receptor dependent synaptically evoked increase in calcium in dendrites, apparently without affecting presynaptic transmitter release. Pharmacological experiments suggest that M1 and M3 receptors are not involved in the mAChR-mediated suppression of tLTP. Taken together, these results suggest activating mAChRs in layer 2/3 intracortical circuits can modify the circuit dynamics of AC by depressing tLTP mediated by NMDA receptors, and depressing calcium influx at excitatory synapses onto layer 2/3 pyramidal cells.

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