Simplified Compartmental Models of CA1 Pyramidal Cells of Theta-Modulated Inhibition Effects on Spike Timing-Dependent Plasticity

2018 ◽  
pp. 645-667
Author(s):  
Vassilis Cutsuridis
Keyword(s):  
Pyramidal Cells ◽  
Compartmental Models ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Ca1 Pyramidal Cells

scholarly journals Input Specificity and Dependence of Spike Timing–Dependent Plasticity on Preceding Postsynaptic Activity at Unitary Connections between Neocortical Layer 2/3 Pyramidal Cells

2009 ◽  
Vol 19 (10) ◽  
pp. 2308-2320 ◽  
Author(s):  
Misha Zilberter ◽  
Carl Holmgren ◽  
Isaac Shemer ◽  
Gilad Silberberg ◽  
Sten Grillner ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Postsynaptic Activity ◽  
Layer 2

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.

Synaptic Democracy in Active Dendrites

2006 ◽  
Vol 96 (5) ◽  
pp. 2307-2318 ◽  
Author(s):  
Clifton C. Rumsey ◽  
L. F. Abbott
Keyword(s):  
Action Potentials ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Spike Timing ◽  
Dominant Factor ◽  
Dependent Plasticity ◽  
Ca1 Pyramidal Cells ◽  
Active Dendrites ◽  
Hebbian Plasticity ◽  
The Impact

Given the extensive attenuation that can occur along dendritic cables, location within the dendritic tree might appear to be a dominant factor in determining the impact of a synapse on the postsynaptic response. By this reasoning, distal synapses should have a smaller effect than proximal ones. However, experimental evidence from several types of neurons, such as CA1 pyramidal cells, indicates that a compensatory strengthening of synapses counteracts the effect of location on synaptic efficacy. A form of spike-timing-dependent plasticity (STDP), called anti-STDP, combined with non-Hebbian activity-dependent plasticity can account for the equalization of synaptic efficacies. This result, obtained originally in models with unbranched passive cables, also arises in multi-compartment models with branched and active dendrites that feature backpropagating action potentials, including models with CA1 pyramidal morphologies. Additionally, when dendrites support the local generation of action potentials, anti-STDP prevents runaway dendritic spiking and locally balances the numbers of dendritic and backpropagating action potentials. Thus in multiple ways, anti-STDP eliminates the location dependence of synapses and allows Hebbian plasticity to operate in a more “democratic” manner.

scholarly journals Effect of Interpopulation Spike-Timing-Dependent Plasticity on Synchronized Rhythms in Neuronal Networks with Inhibitory and Excitatory Populations

2019 ◽  
Author(s):  
Sang-Yoon Kim ◽  
Woochang Lim
Keyword(s):  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Term Potentiation ◽  
Wide Range ◽  
Raster Plot ◽  
Average Fraction

We consider a two-population network consisting of both inhibitory (I) interneurons and excitatory (E) pyramidal cells. This I-E neuronal network has adaptive dynamic I to E and E to I interpopulation synaptic strengths, governed by interpopulation spike-timing-dependent plasticity (STDP). In previous works without STDPs, fast sparsely synchronized rhythms, related to diverse cognitive functions, were found to appear in a range of noise intensity D for static synaptic strengths. Here, by varying D, we investigate the effect of interpopulation STDPs on fast sparsely synchronized rhythms that emerge in both the I- and the E-populations. Depending on values of D, long-term potentiation (LTP) and long-term depression (LTD) for population-averaged values of saturated interpopulation synaptic strengths are found to occur. Then, the degree of fast sparse synchronization varies due to effects of LTP and LTD. In a broad region of intermediate D, the degree of good synchronization (with higher synchronization degree) becomes decreased, while in a region of large D, the degree of bad synchronization (with lower synchronization degree) gets increased. Consequently, in each I- or E-population, the synchronization degree becomes nearly the same in a wide range of D (including both the intermediate and the large D regions). This kind of “equalization effect” is found to occur via cooperative interplay between the average occupation and pacing degrees of spikes (i.e., the average fraction of firing neurons and the average degree of phase coherence between spikes in each synchronized stripe of spikes in the raster plot of spikes) in fast sparsely synchronized rhythms. Finally, emergences of LTP and LTD of interpopulation synaptic strengths (leading to occurrence of equalization effect) are intensively investigated via a microscopic method based on the distributions of time delays between the pre- and the post-synaptic spike times.PACS numbers87.19.lw, 87.19.lm, 87.19.lc

Stable Competitive Dynamics Emerge from Multispike Interactions in a Stochastic Model of Spike-Timing-Dependent Plasticity

2006 ◽  
Vol 18 (10) ◽  
pp. 2414-2464 ◽  
Author(s):  
Peter A. Appleby ◽  
Terry Elliott
Keyword(s):  
Synaptic Plasticity ◽  
Stochastic Model ◽  
Higher Order ◽  
Spike Timing ◽  
Competitive Dynamics ◽  
Spike Timing Dependent Plasticity ◽  
Interaction Function ◽  
Dependent Plasticity ◽  
Order Interaction ◽  
Synaptic Dynamics

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.

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