scholarly journals Spike timing-dependent plasticity: a learning rule for dendritic integration in rat CA1 pyramidal neurons

2008 ◽  
Vol 586 (3) ◽  
pp. 779-793 ◽  
Author(s):  
Emilie Campanac ◽  
Dominique Debanne
Keyword(s):  
Pyramidal Neurons ◽  
Learning Rule ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dendritic Integration ◽  
Dependent Plasticity ◽  
Ca1 Pyramidal Neurons

Supervised Spike-Timing-Dependent Plasticity: A Spatiotemporal Neuronal Learning Rule for Function Approximation and Decisions

2013 ◽  
Vol 25 (12) ◽  
pp. 3113-3130 ◽  
Author(s):  
Jan-Moritz P. Franosch ◽  
Sebastian Urban ◽  
J. Leo van Hemmen
Keyword(s):  
Function Approximation ◽  
Sensory Input ◽  
Learning Rule ◽  
Animal Learn ◽  
Spike Timing ◽  
Time Dependent ◽  
Stable Configuration ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Tactile System

How can an animal learn from experience? How can it train sensors, such as the auditory or tactile system, based on other sensory input such as the visual system? Supervised spike-timing-dependent plasticity (supervised STDP) is a possible answer. Supervised STDP trains one modality using input from another one as “supervisor.” Quite complex time-dependent relationships between the senses can be learned. Here we prove that under very general conditions, supervised STDP converges to a stable configuration of synaptic weights leading to a reconstruction of primary sensory input.

scholarly journals Beyond spike-timing-dependent plasticity: a computational study of plasticity gradients across basal dendrites

2016 ◽  
Author(s):  
Jacopo Bono ◽  
Claudia Clopath
Keyword(s):  
Synaptic Plasticity ◽  
Computational Study ◽  
Learning Rule ◽  
Spike Timing ◽  
Memory Retention ◽  
Neuron Models ◽  
Spike Timing Dependent Plasticity ◽  
Principal Mechanism ◽  
Dependent Plasticity ◽  
Dendritic Spikes

AbstractSynaptic plasticity is thought to be the principal mechanism underlying learning in the brain. Models of plastic networks typically combine point neurons with spike-timing-dependent plasticity (STDP) as the learning rule. However, a point neuron does not capture the complexity of dendrites, which allow non-linear local processing of the synaptic inputs. Furthermore, experimental evidence suggests that STDP is not the only learning rule available to neurons. Implementing biophysically realistic neuron models, we studied how dendrites allow for multiple synaptic plasticity mechanisms to coexist in a single cell. In these models, we compared the conditions for STDP and for the synaptic strengthening by local dendritic spikes. We further explored how the connectivity between two cells is affected by these plasticity rules and the synaptic distributions. Finally, we show how memory retention in associative learning can be prolonged in networks of neurons with dendrites.

Role of AMPA and NMDA Receptors and Back-Propagating Action Potentials in Spike Timing–Dependent Plasticity

2010 ◽  
Vol 103 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Marco Fuenzalida ◽  
David Fernández de Sevilla ◽  
Alejandro Couve ◽  
Washington Buño
Keyword(s):  
Nmda Receptors ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Cellular Mechanisms ◽  
Dependent Plasticity ◽  
Term Potentiation

The cellular mechanisms that mediate spike timing–dependent plasticity (STDP) are largely unknown. We studied in vitro in CA1 pyramidal neurons the contribution of AMPA and N-methyl-d-aspartate (NMDA) components of Schaffer collateral (SC) excitatory postsynaptic potentials (EPSPs; EPSPAMPA and EPSPNMDA) and of the back-propagating action potential (BAP) to the long-term potentiation (LTP) induced by a STDP protocol that consisted in pairing an EPSP and a BAP. Transient blockade of EPSPAMPA with 7-nitro-2,3-dioxo-1,4-dihydroquinoxaline-6-carbonitrile (CNQX) during the STDP protocol prevented LTP. Contrastingly LTP was induced under transient inhibition of EPSPAMPA by combining SC stimulation, an imposed EPSPAMPA-like depolarization, and BAP or by coupling the EPSPNMDA evoked under sustained depolarization (approximately −40 mV) and BAP. In Mg2+-free solution EPSPNMDA and BAP also produced LTP. Suppression of EPSPNMDA or BAP always prevented LTP. Thus activation of NMDA receptors and BAPs are needed but not sufficient because AMPA receptor activation is also obligatory for STDP. However, a transient depolarization of another origin that unblocks NMDA receptors and a BAP may also trigger LTP.

scholarly journals A spike-timing-dependent plasticity rule for single, clustered and distributed dendritic spines

2018 ◽  
Author(s):  
Sabrina Tazerart ◽  
Diana E. Mitchell ◽  
Soledad Miranda-Rottmann ◽  
Roberto Araya
Keyword(s):  
Dendritic Spines ◽  
Actin Polymerization ◽  
Pyramidal Neurons ◽  
Glutamate Release ◽  
Synaptic Strength ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Spine Shape ◽  
Stdp Rule

SUMMARYSpike-timing-dependent plasticity (STDP) has been extensively studied in cortical pyramidal neurons, however, the precise structural organization of excitatory inputs that supports STDP, as well as the structural, molecular and functional properties of dendritic spines during STDP remain unknown. Here we performed a spine STDP protocol using two-photon glutamate uncaging to mimic presynaptic glutamate release (pre) paired with somatically generated postsynaptic spikes (post). We found that the induction of STDP in single spines follows a classical Hebbian STDP rule, where pre-post pairings at timings that trigger LTP (t-LTP) produce shrinkage of the activated spine neck and a concomitant increase in its synaptic strength; and post-pre pairings that trigger LTD (t-LTD) decrease synaptic strength without affecting the activated spine shape. Furthermore, we tested whether the single spine-Hebbian STDP rule could be affected by the activation of neighboring (clustered) or distant (distributed) spines. Our results show that the induction of t-LTP in two clustered spines (<5 μm apart) enhances LTP through a mechanism dependent on local spine calcium accumulation and actin polymerization-dependent neck shrinkage, whereas t-LTD was disrupted by the activation of two clustered spines but recovered when spines were separated by >40 μm. These results indicate that synaptic cooperativity, induced by the co-activation of only two clustered spines, provides local dendritic depolarization and local calcium signals sufficient to disrupt t-LTD and extend the temporal window for the induction of t-LTP, leading to STDP only encompassing LTP.

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