Requirement of an Allosteric Kinetics of NMDA Receptors for Spike Timing-Dependent Plasticity

Urakubo, Hidetoshi; Honda, Masaki; Froemke, Robert C.; Kuroda, Shinya

doi:10.1523/jneurosci.0303-08.2008

Cited by 73 publications

(110 citation statements)

References 141 publications

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“…If we apply the same STDP model not only to RGC-TN synapses but also to TN-TN synapses, all of the TN-TN synapses may be potentiated by the repetitive exposure of the retina to the fast-moving light bar. This corresponds to the situation in which burst firings in both pre-neurons and postneurons lead to potentiation, regardless of the order of the firings in pre-neurons and post-neurons (Froemke et al, 2006;Urakubo et al, 2008). In this case with STDP at TN-TN synapses, stronger early transient feedforward signals and the decrease in the transition threshold of feedback excitation due to the potentiation of all TN-TN synapses are similarly likely to lead to the development of direction selectivity.…”

Section: Stdp In Tn-tn Synapsesmentioning

confidence: 93%

“…Synaptic modification was induced through STDP in the synapses from the RGCs to the TNs. As a synaptic learning rule, we used a simple STDP model, which was made by simplifying the detailed molecular STDP model (Urakubo et al, 2008. A detailed description of the simple STDP model is provided in the supplemental material (available at www.jneurosci.org).…”

Section: Methodsmentioning

confidence: 99%

“…1 A, B) (see Materials and Methods). The simple STDP model was made using a simplification of a detailed molecular STDP model (Urakubo et al, 2008) to reduce the computational cost. We determined the structure of the neural circuit in the retinotectal circuit model by extracting essential knowledge to explain the development of direction selectivity from experimental findings (Rybicka and Udin, 1994;Tao and Poo, 2005;Akerman and Cline, 2006;Lien et al, 2006;Pratt et al, 2008).…”

Section: Construction Of the Retinotectal Circuit Modelmentioning

confidence: 99%

“…We constructed a realistic neural circuit model of the Xenopus retinotectal system that could be quantitatively compared with various observed experimental features (Engert et al, 2002). To incorporate a synaptic learning rule, we simplified the detailed molecular STDP model (Urakubo et al, 2008) to produce a simple STDP model that retained the ability to reproduce the experimentally observed temporally asymmetric learning window ( Fig. 1B; supplemental Fig.…”

Section: Introductionmentioning

confidence: 99%

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Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

Honda¹,

Urakubo²,

Tanaka³

et al. 2011

J. Neurosci.

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The development of direction selectivity in the visual system depends on visual experience. In the developing Xenopus retinotectal system, tectal neurons (TNs) become direction selective through spike timing-dependent plasticity (STDP) after repetitive retinal exposure to a moving bar in a specific direction. We investigated the mechanism responsible for the development of direction selectivity in the Xenopus retinotectal system using a neural circuit model with STDP. In this retinotectal circuit model, a moving bar stimulated the retinal ganglion cells (RGCs), which provided feedforward excitation to the TNs and interneurons (INs). The INs provided delayed feedforward inhibition to the TNs. The TNs also received feedback excitation from neighboring TNs. As a synaptic learning rule, a molecular STDP model was used for synapses between the RGCs and TNs. The retinotectal circuit model reproduced experimentally observed features of the development of direction selectivity, such as increase in input to the TN. The peak of feedforward excitation from RGCs to TNs shifted earlier as a result of STDP. Together with the delayed feedforward inhibition, a stronger earlier transient feedforward signal was generated, which exceeded the threshold of the feedback excitation from the neighboring TNs and resulted in amplification of input to the TN. The suppression of the delayed feedforward inhibition resulted in the development of orientation selectivity rather than direction selectivity, indicating the pivotal role of the delayed feedforward inhibition in direction selectivity. We propose a mechanism for the development of direction selectivity involving a delayed feedforward inhibition with STDP and the amplification of feedback excitation.

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Section: Stdp In Tn-tn Synapsesmentioning

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Section: Construction Of the Retinotectal Circuit Modelmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

Honda¹,

Urakubo²,

Tanaka³

et al. 2011

J. Neurosci.

Self Cite

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“…It is very difficult to test this conjecture experimentally. It has also been suggested that one of several alternative mechanisms may serve as the second coincidence detector required for the induction of LTD by spike and triplet pairing stimulation protocols [42,45,66]. By elaborating the secondary messenger pathways in the plasticity model to more closely replicate the activity of CaM, CaMKII, PP1, PP2A, I1 and other proteins implicated in plasticity expression, as well as additional sources of internal and external Calcium influx, it may be possible to more accurately appraise the contributions made by bAPs to synaptic plasticity [7,46,67].…”

Section: Discussionmentioning

confidence: 99%

Calcium control of triphasic hippocampal STDP

Bush¹,

Jin

2012

J Comput Neurosci

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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...

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Long-Term Plasticity, Biophysical Models

Clopath

2022

Encyclopedia of Computational Neuroscience

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Requirement of an Allosteric Kinetics of NMDA Receptors for Spike Timing-Dependent Plasticity

Cited by 73 publications

References 141 publications

Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

Analysis of Development of Direction Selectivity in Retinotectum by a Neural Circuit Model with Spike Timing-Dependent Plasticity

Calcium control of triphasic hippocampal STDP

Long-Term Plasticity, Biophysical Models

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