Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Spike-timing control by dendritic plateau potentials in the presence of synaptic barrages.

ABSTRACT: Apical and tuft dendrites of pyramidal neurons support regenerative electrical potentials, giving rise to long-lasting (approximately hundreds of milliseconds) and strong (~50 mV from rest) depolarizations. Such plateau events rely on clustered glutamatergic input, can be mediated by calcium or by NMDA currents, and often generate somatic depolarizations that last for the time course of the dendritic plateau event. We address the computational significance of such single-neuron processing via reduced but biophysically realistic modeling. We introduce a model based on two discrete integration zones, a somatic and a dendritic one, that communicate from the dendritic to the somatic compartment via a long plateau-conductance. We show principled differences in the way dendritic vs. somatic inhibition controls spike timing, and demonstrate how this could implement spike time control in the face of barrages of synaptic inputs.

SUBMITTER: Shai AS

PROVIDER: S-EPMC4132263 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Spike-timing control by dendritic plateau potentials in the presence of synaptic barrages.

Shai Adam S AS Koch Christof C Anastassiou Costas A CA

Frontiers in computational neuroscience 20140814

Apical and tuft dendrites of pyramidal neurons support regenerative electrical potentials, giving rise to long-lasting (approximately hundreds of milliseconds) and strong (~50 mV from rest) depolarizations. Such plateau events rely on clustered glutamatergic input, can be mediated by calcium or by NMDA currents, and often generate somatic depolarizations that last for the time course of the dendritic plateau event. We address the computational significance of such single-neuron processing via re ...[more]

PMID: 25177288

Similar Datasets

Dendritic small conductance calcium-activated potassium channels activated by action potentials suppress EPSPs and gate spike-timing dependent synaptic plasticity.

Project description:Small conductance calcium-activated potassium channels (SK channels) are present in spines and can be activated by backpropagating action potentials (APs). This suggests they may play a critical role in spike-timing dependent synaptic plasticity (STDP). Consistent with this idea, EPSPs in both cortical and hippocampal pyramidal neurons were suppressed by preceding APs in an SK-dependent manner. In cortical pyramidal neurons EPSP suppression by preceding APs depended on their precise timing as well as the distance of activated synapses from the soma, was dendritic in origin, and involved SK-dependent suppression of NMDA receptor activation. As a result SK channel activation by backpropagating APs gated STDP induction during low-frequency AP-EPSP pairing, with both LTP and LTD absent under control conditions but present after SK channel block. These findings indicate that activation of SK channels in spines by backpropagating APs plays a key role in regulating both EPSP amplitude and STDP induction.

| S-EPMC5679750 | biostudies-literature

Neuromodulators control the polarity of spike-timing-dependent synaptic plasticity.

Project description:Near coincidental pre- and postsynaptic action potentials induce associative long-term potentiation (LTP) or long-term depression (LTD), depending on the order of their timing. Here, we show that in visual cortex the rules of this spike-timing-dependent plasticity are not rigid, but shaped by neuromodulator receptors coupled to adenylyl cyclase (AC) and phospholipase C (PLC) signaling cascades. Activation of the AC and PLC cascades results in phosphorylation of postsynaptic glutamate receptors at sites that serve as specific "tags" for LTP and LTD. As a consequence, the outcome (i.e., whether LTP or LTD) of a given pattern of pre- and postsynaptic firing depends not only on the order of the timing, but also on the relative activation of neuromodulator receptors coupled to AC and PLC. These findings indicate that cholinergic and adrenergic neuromodulation associated with the behavioral state of the animal can control the gating and the polarity of cortical plasticity.

| S-EPMC2756178 | biostudies-literature

Attenuation of Synaptic Potentials in Dendritic Spines.

Project description:Dendritic spines receive the majority of excitatory inputs in many mammalian neurons, but their biophysical properties and exact role in dendritic integration are still unclear. Here, we study spine electrical properties in cultured hippocampal neurons using an improved genetically encoded voltage indicator (ArcLight) and two-photon glutamate uncaging. We find that back-propagating action potentials (bAPs) fully invade dendritic spines. However, uncaging excitatory post-synaptic potentials (uEPSPs) generated by glutamate photorelease, ranging from 4 to 27 mV in amplitude, are attenuated by up to 4-fold as they propagate to the parent dendrites. Finally, the simultaneous occurrence of bAPs and uEPSPs results in sublinear summation of membrane potential. Our results demonstrate that spines can behave as electric compartments, reducing the synaptic inputs injected into the cell, while receiving bAPs are unmodified. The attenuation of EPSPs by spines could have important repercussions for synaptic plasticity and dendritic integration.

| S-EPMC5709047 | biostudies-literature

Electrodiffusion models of synaptic potentials in dendritic spines.

Project description:The biophysical properties of dendritic spines play a critical role in neuronal integration but are still poorly understood, due to experimental difficulties in accessing them. Spine biophysics has been traditionally explored using theoretical models based on cable theory. However, cable theory generally assumes that concentration changes associated with ionic currents are negligible and, therefore, ignores electrodiffusion, i.e. the interaction between electric fields and ionic diffusion. This assumption, while true for large neuronal compartments, could be incorrect when applied to femto-liter size structures such as dendritic spines. To extend cable theory and explore electrodiffusion effects, we use here the Poisson (P) and Nernst-Planck (NP) equations, which relate electric field to charge and Fick's law of diffusion, to model ion concentration dynamics in spines receiving excitatory synaptic potentials (EPSPs). We use experimentally measured voltage transients from spines with nanoelectrodes to explore these dynamics with realistic parameters. We find that (i) passive diffusion and electrodiffusion jointly affect the dynamics of spine EPSPs; (ii) spine geometry plays a key role in shaping EPSPs; and, (iii) the spine-neck resistance dynamically decreases during EPSPs, leading to short-term synaptic facilitation. Our formulation, which complements and extends cable theory, can be easily adapted to model ionic biophysics in other nanoscale bio-compartments.

| S-EPMC7350286 | biostudies-literature

Adrenergic Gate Release for Spike Timing-Dependent Synaptic Potentiation.

Project description:Spike timing-dependent synaptic plasticity (STDP) serves as a key cellular correlate of associative learning, which is facilitated by elevated attentional and emotional states involving activation of adrenergic signaling. At cellular levels, adrenergic signaling increases dendrite excitability, but the underlying mechanisms remain elusive. Here we show that activation of ?2-adrenoceptors promoted STD long-term synaptic potentiation at mouse hippocampal excitatory synapses by inactivating dendritic Kv1.1-containing potassium channels, which increased dendrite excitability and facilitated dendritic propagation of postsynaptic depolarization, potentially improving coincidental activation of pre- and postsynaptic terminals. We further demonstrate that adrenergic modulation of Kv1.1 was mediated by the signaling scaffold SAP97, which, through direct protein-protein interactions, escorts ?2 signaling to remove Kv1.1 from the dendrite surface. These results reveal a mechanism through which the postsynaptic signaling scaffolds bridge the aroused brain state to promote induction of synaptic plasticity and potentially to enhance spike timing and memory encoding.

| S-EPMC5267933 | biostudies-literature

Memory-Efficient Synaptic Connectivity for Spike-Timing- Dependent Plasticity.

Project description:Spike-Timing-Dependent Plasticity (STDP) is a bio-inspired local incremental weight update rule commonly used for online learning in spike-based neuromorphic systems. In STDP, the intensity of long-term potentiation and depression in synaptic efficacy (weight) between neurons is expressed as a function of the relative timing between pre- and post-synaptic action potentials (spikes), while the polarity of change is dependent on the order (causality) of the spikes. Online STDP weight updates for causal and acausal relative spike times are activated at the onset of post- and pre-synaptic spike events, respectively, implying access to synaptic connectivity both in forward (pre-to-post) and reverse (post-to-pre) directions. Here we study the impact of different arrangements of synaptic connectivity tables on weight storage and STDP updates for large-scale neuromorphic systems. We analyze the memory efficiency for varying degrees of density in synaptic connectivity, ranging from crossbar arrays for full connectivity to pointer-based lookup for sparse connectivity. The study includes comparison of storage and access costs and efficiencies for each memory arrangement, along with a trade-off analysis of the benefits of each data structure depending on application requirements and budget. Finally, we present an alternative formulation of STDP via a delayed causal update mechanism that permits efficient weight access, requiring no more than forward connectivity lookup. We show functional equivalence of the delayed causal updates to the original STDP formulation, with substantial savings in storage and access costs and efficiencies for networks with sparse synaptic connectivity as typically encountered in large-scale models in computational neuroscience.

| S-EPMC6499189 | biostudies-literature

A spike-timing-dependent plasticity rule for dendritic spines.

Project description:The structural organization of excitatory inputs supporting spike-timing-dependent plasticity (STDP) remains unknown. We performed a spine STDP protocol using two-photon (2P) glutamate uncaging (pre) paired with postsynaptic spikes (post) in layer 5 pyramidal neurons from juvenile mice. Here we report that pre-post pairings that trigger timing-dependent LTP (t-LTP) produce shrinkage of the activated spine neck and increase in synaptic strength; and post-pre pairings that trigger timing-dependent LTD (t-LTD) decrease synaptic strength without affecting spine shape. Furthermore, the induction of t-LTP with 2P glutamate uncaging in clustered spines (<5 μm apart) enhances LTP through a NMDA receptor-mediated spine calcium accumulation and actin polymerization-dependent neck shrinkage, whereas t-LTD was dependent on NMDA receptors and disrupted by the activation of clustered spines but recovered when separated by >40 μm. These results indicate that synaptic cooperativity disrupts t-LTD and extends the temporal window for the induction of t-LTP, leading to STDP only encompassing LTP.

| S-EPMC7449969 | biostudies-literature

Spike-shape dependence of the spike-timing dependent synaptic plasticity in ferroelectric-tunnel-junction synapses.

Project description:Resistive switching (RS) devices have attracted increasing attention for artificial synapse applications in neural networks because of their nonvolatile and analogue resistance changes. Among the neural networks, a spiking neural network (SNN) based on spike-timing-dependent plasticity (STDP) is highly energy efficient. To implement STDP in resistive switching devices, several types of voltage spikes have been proposed to date, but there have been few reports on the relationship between the STDP characteristics and spike types. Here, we report the STDP characteristics implemented in ferroelectric tunnel junctions (FTJs) by several types of spikes. Based on simulated time evolutions of superimposed spikes and taking the nonlinear current-voltage (I-V) characteristics of FTJs into account, we propose equations for simulating the STDP curve parameters of a magnitude of the conductance change (?Gmax) and a time window (?C) from the spike parameters of a peak amplitude (Vpeak) and time durations (tp and td) for three spike types: triangle-triangle, rectangular-triangle, and rectangular-rectangular. The power consumption experiments of the STDP revealed that the power consumption under the inactive-synapse condition (spike timing |?t|?>??C) was as large as 50-82% of that under the active-synapse condition (|?t|?<??C). This finding indicates that the power consumption under the inactive-synapse condition should be reduced to minimize the total power consumption of an SNN implemented by using FTJs as synapses.

| S-EPMC6882828 | biostudies-literature

Multiple topological representation self-organized by spike-timing-dependent synaptic learning rule.

Project description:Position-and-scale-free representations of shapes are acquired by neurons in the inferior temporal (IT) cortex. So each neuron receives information from the whole visual field. Familiar shapes are extremely restricted from all the possible shapes on the whole visual field. So they must be clustered in the shape space to have mixed structure of continuity and discreteness. We demonstrate that multiple representation can be acquired in a spike-based model for topological maps based on the spike-timing-dependent synaptic plasticity (STDP), subjected to a set of inputs on multiple rings, which is a simple example of mixed structure. In this representation, the position on each ring is represented by a center of active neurons and the difference of rings is represented by a detailed pattern of active neurons. Neurons in the same region exhibit high activities for an input on the other ring. The result is consistent with the fact observed in IT cortex that neighboring neurons exhibit different preferences while the region of active neurons is continuously shifted for continuous changes of object.

| S-EPMC2645499 | biostudies-other

Inferior Olive HCN1 Channels Coordinate Synaptic Integration and Complex Spike Timing.

Project description:Cerebellar climbing-fiber-mediated complex spikes originate from neurons in the inferior olive (IO), are critical for motor coordination, and are central to theories of cerebellar learning. Hyperpolarization-activated cyclic-nucleotide-gated (HCN) channels expressed by IO neurons have been considered as pacemaker currents important for oscillatory and resonant dynamics. Here, we demonstrate that in vitro, network actions of HCN1 channels enable bidirectional glutamatergic synaptic responses, while local actions of HCN1 channels determine the timing and waveform of synaptically driven action potentials. These roles are distinct from, and may complement, proposed pacemaker functions of HCN channels. We find that in behaving animals HCN1 channels reduce variability in the timing of cerebellar complex spikes, which serve as a readout of IO spiking. Our results suggest that spatially distributed actions of HCN1 channels enable the IO to implement network-wide rules for synaptic integration that modulate the timing of cerebellar climbing fiber signals.

| S-EPMC5847187 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data