Spine Ca<sup>2+</sup>Signaling in Spike-Timing-Dependent Plasticity

Nevian, Thomas; Sakmann, Bert

doi:10.1523/jneurosci.1749-06.2006

Cited by 421 publications

(608 citation statements)

References 92 publications

Supporting

Mentioning

559

Contrasting

Unclassified

Order By: Relevance

“…Indeed, for spike coding (and without subthreshold voltage manipulations) our plasticity rule behaves like a STDP rule where triplets of spikes with pre--post--post or post--pre--post timing evoke LTP 28--29 , whereas pairs with post--pre timing evoke LTD. In contrast to standard STDP rules (reviewed in 16 ), pairing frequency dependence 18 and burst--timing dependence 32 are qualitatively described. In addition the rule is expected to reproduce the triplet and quadruplet experiments in hippocampal slices 40 (data not shown), because for all STDP protocols the plasticity rule in this paper is similar to an earlier nonlinear STDP rule 29 .…”

Section: Discussionmentioning

confidence: 73%

“…Both the ``potentiation is rescued by depolarization'' 18 scenario (Fig. 2f) and that of burst--timing dependent LTP 32 (Fig. 3) show that LTP at low frequency is induced when the membrane is depolarized before the pre--post pairing.…”

Section: Discussionmentioning

confidence: 90%

“…3) show that LTP at low frequency is induced when the membrane is depolarized before the pre--post pairing. This depolarization can be due to a previous spike during a postsynaptic burst 32 or to a depolarization current. A further unexpected result is that, with the set of parameters derived from visual cortex slice experiments, synapses fluctuate rapidly between strong and weak weights.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Connectivity reflects coding: a model of voltage-based STDP with homeostasis

et al. 2010

View full text Add to dashboard Cite

Electrophysiological connectivity patterns in cortex often show a few strong connections, sometimes bidirectional, in a sea of weak connections. In order to explain these connectivity patterns, we use a model of Spike--Timing--Dependent Plasticity where synaptic changes depend on presynaptic spike arrival and the postsynaptic membrane potential, filtered with two different time constants. The model describes several nonlinear effects in STDP experiments, as well as the voltage dependence of plasticity. We show that in a simulated recurrent network of spiking neurons our plasticity rule leads not only to development of localized receptive fields, but also to connectivity patterns that reflect the neural code: for temporal coding paradigms with spatio--temporal input correlations, strong connections are predominantly unidirectional, whereas they are bidirectional under rate coded input with spatial correlations only. Thus variable connectivity patterns in the brain could reflect different coding principles across brain areas; moreover simulations suggest that plasticity is surprisingly fast.

show abstract

Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Connectivity reflects coding: a model of voltage-based STDP with homeostasis

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Indeed, not only LTSs mediate large Ca 2C entry but also since T-type channels deactivate slowly, the calcium influx associated to the potential recruitment of T-type currents during brief depolarizing events, such as back-propagating action potentials or fast synaptic events, is especially large 42,43 and mediate significant dendritic Ca 2C rises. However, to the best of our knowledge, the requirement of a specific funneling of Ca 2C through T-type channels as a prerequisite to induce synaptic plasticity was seldom investigated 44 and only demonstrated at the inhibitory synapse between neurons of the nucleus reticularis thalami (NRT) and thalamocortical neurons of the ventrobasal somatosensory nucleus (Fig. 1A, synapse 1).…”

Section: Activation Of T-type Channels Mediates Membrane Depolarizatimentioning

confidence: 99%

T-type calcium channels in synaptic plasticity

Leresche

Lambert

2016

Channels

View full text Add to dashboard Cite

The role of T-type calcium currents is rarely considered in the extensive literature covering the mechanisms of long-term synaptic plasticity. This situation reflects the lack of suitable T-type channel antagonists that till recently has hampered investigations of the functional roles of these channels. However, with the development of new pharmacological and genetic tools, a clear involvement of T-type channels in synaptic plasticity is starting to emerge. Here, we review a number of studies showing that T-type channels participate to numerous homo-and heterosynaptic plasticity mechanisms that involve different molecular partners and both pre-and postsynaptic modifications. The existence of T-channel dependent and independent plasticity at the same synapse strongly suggests a subcellular localization of these channels and their partners that allows specific interactions. Moreover, we illustrate the functional importance of T-channel dependent synaptic plasticity in neocortex and thalamus.

show abstract

“…Experimental studies have demonstrated that the Calcium control hypothesis does not hold true for excitatory synapses between cortical pyramidal cells -at which there is no evidence for the existence of a triphasic STDP rule. A variety of alternative mechanisms, including metabotropic glutamate receptor, pre-synaptic NMDAr and retrograde endocannabinoid signalling, have been implicated in the induction of LTD by spike-timing stimulation protocols in cortex [77][78][79][80]. It seems likely that this dichotomy in synaptic plasticity mechanisms between cortex and hippocampus might both reflect and be reflected by functional differences in neural processing mediated by these regions.…”

Section: Discussionmentioning

confidence: 99%

Calcium control of triphasic hippocampal STDP

Bush¹,

Jin

2012

J Comput Neurosci

View full text Add to dashboard Cite

Synaptic plasticity is believed to represent the neural correlate of mammalian learning and memory function. It has been demonstrated that changes in synaptic conductance can be induced by approximately synchronous pairings of pre-and post-synaptic action potentials delivered at low frequencies. It has also been established that NMDAr-dependent Calcium influx into dendritic spines represents the critical signal for plasticity induction, and can account for this spike-timing dependent plasticity (STDP) as well as experimental data obtained using other stimulation protocols. However, subsequent empirical studies have delineated a more complex relationship between spike-timing, firing rate, stimulus duration and post-synaptic bursting in dictating changes in the conductance of hippocampal excitatory synapses. It has yet to be established whether the Calcium control hypothesis can account for this more recent data. Here, we present a detailed biophysical model of single dendritic spines on a CA1 pyramidal neuron, describe the NMDAr-dependent Calcium influx generated by different stimulation protocols, and present a parsimonious model of Calcium driven kinase and phosphotase dynamics that dictate transitions between binary synaptic weight states. We demonstrate the manner in which this model can account for various experimental observations of synaptic plasticity and be used to make predictions regarding the dynamics of depolarisation and NMDAr activation generated by STDP protocols as well as the synaptic weight change induced under other experimental conditions. We then discuss how this parsimonious, unified computational model of synaptic plasticity might be utilised to appraise the activity-dependent refinement of neural circuitry induced by more realistic firing patterns. IntroductionSynaptic plasticity -the process of activity dependent change in synaptic conductance -is widely believed to represent the neural correlate of mammalian learning and memory function [1][2][3]. Since the first experimental demonstrations of long-term potentiation (LTP) and depression (LTD), a wealth of empirical data regarding the induction, expression and maintenance of synaptic plasticity in different cortical regions has been obtained [4][5][6][7][8]. In spite of the heterogeneity of plasticity mechanisms observed throughout the brain, changes in the strength of excitatory synapses afferent on CA1 pyramidal neurons in the hippocampus represent the best studied form in the mammalian cortex [9][10][11][12]. At these synapses, Calcium influx into dendritic spines represents the critical signal for synaptic plasticity induction [13][14][15][16][17][18][19][20]. Large, transient elevations in intracellular [Ca 2+ ] generate LTP via the preferential activation of kinase pathways while modest, sustained elevations in intracellular [Ca 2+ ] generate LTD via the preferential activation of phosphotase pathways [21][22][23][24][25]. Initially, empirical observations of synaptic plasticity were mediated by tetanic stimulation protoc...

show abstract

Spine Ca²⁺Signaling in Spike-Timing-Dependent Plasticity

Cited by 421 publications

References 92 publications

Connectivity reflects coding: a model of voltage-based STDP with homeostasis

Connectivity reflects coding: a model of voltage-based STDP with homeostasis

T-type calcium channels in synaptic plasticity

Calcium control of triphasic hippocampal STDP

Contact Info

Product

Resources

About

Spine Ca2+Signaling in Spike-Timing-Dependent Plasticity

Cited by 421 publications

References 92 publications

Connectivity reflects coding: a model of voltage-based STDP with homeostasis

Connectivity reflects coding: a model of voltage-based STDP with homeostasis

T-type calcium channels in synaptic plasticity

Calcium control of triphasic hippocampal STDP

Contact Info

Product

Resources

About

Spine Ca²⁺Signaling in Spike-Timing-Dependent Plasticity