Synaptic Activity Modulates the Induction of Bidirectional Synaptic Changes in Adult Mouse Hippocampus

Ngezahayo, Anaclet; Schachner, Melitta; Artola, Alain

doi:10.1523/jneurosci.20-07-02451.2000

Cited by 131 publications

(142 citation statements)

References 54 publications

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“…Consistent with voltage clamp 12 and stationary depolarization experiment 11 , LTD is triggered in our model if presynaptic spike arrival occurs while the membrane potential of the postsynaptic neuron is slightly depolarized (above a threshold θ --usually set to resting potential) whereas LTP occurs if depolarization is big (above a second threshold θ + , see Fig. 1).…”

Section: Fitting the Plasticity Model To Experimental Datasupporting

confidence: 76%

“…The total number of parameters of the plasticity model is then 7. For all data sets, except the one taken from 12 , the threshold is set to the resting potential and to the firing threshold of the AdEx model, i.e.…”

Section: Parameters and Data Fittingmentioning

confidence: 99%

“…For the data set in hippocampus 12 , we also fit the two parameters and since completely different preparations and cell type were used. Moreover for this data set, the time constant τ x is taken from physiological measurements given in 10 and fixed to the values of 16ms.…”

Section: Parameters and Data Fittingmentioning

confidence: 99%

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

et al. 2010

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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.

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Section: Fitting the Plasticity Model To Experimental Datasupporting

confidence: 76%

Section: Parameters and Data Fittingmentioning

confidence: 99%

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

et al. 2010

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“…In each case, this model qualitatively replicates experimental data and the results of previous modelling studies -both solely pre-synaptic TBS and simultaneous pre-and postsynaptic TBS generating saturated LTP with a final synaptic weight of 1.89 ± 0.01 [48,[60][61][62].…”

Section: Induction Of Synaptic Plasticity By Other Stimulation Protocolssupporting

confidence: 79%

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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“…However, LTP and LTD can also be induced at the same stimulus frequency. This phenomenon has been demonstrated at hippocampal, neocortical, and cerebellar synapses, where potentiation and depression mechanisms operate over a wide range of activation frequencies (2)(3)(4)(5)(6)(7). In the neocortex and hippocampus, the level of postsynaptic depolarization determines whether LTP or LTD results from stimulation at a given frequency (2,5).…”

mentioning

confidence: 96%

Calcium threshold shift enables frequency-independent control of plasticity by an instructive signal

Piochon

Titley

Simmons

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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At glutamatergic synapses, both long-term potentiation (LTP) and long-term depression (LTD) can be induced at the same synaptic activation frequency. Instructive signals determine whether LTP or LTD is induced, by modulating local calcium transients. Synapses maintain the ability to potentiate or depress over a wide frequency range, but it remains unknown how calcium-controlled plasticity operates when frequency variations alone cause differences in calcium amplitudes. We addressed this problem at cerebellar parallel fiber-Purkinje cell synapses, which can undergo LTD or LTP in response to 1-Hz and 100-Hz stimulation. We observed that high-frequency activation elicits larger spine calcium transients than low-frequency stimulation under all stimulus conditions, but, regardless of activation frequency, climbing fiber (CF) coactivation provides an instructive signal that further enhances calcium transients and promotes LTD. At both frequencies, buffering calcium prevents LTD induction and LTP results instead, identifying the enhanced calcium signal amplitude as the critical parameter contributed by the instructive CF signal. These observations show that it is not absolute calcium amplitudes that determine whether LTD or LTP is evoked but, instead, the LTD threshold slides, thus preserving the requirement for relatively larger calcium transients for LTD than for LTP induction at any given stimulus frequency. Cerebellar LTD depends on the activation of calcium/ calmodulin-dependent kinase II (CaMKII). Using genetically modified (TT305/6VA and T305D) mice, we identified α-CaMKII inhibition upon autophosphorylation at Thr305/306 as a molecular event underlying the threshold shift. This mechanism enables frequencyindependent plasticity control by the instructive CF signal based on relative, not absolute, calcium thresholds.S ynaptic activation frequency is an important factor in the induction of long-term potentiation (LTP) and long-term depression (LTD). For example, it has been shown at Schaffer collateral-CA1 pyramidal cell synapses that application of 900 pulses at 1-3 Hz causes LTD, whereas the same number of pulses applied at 50 Hz causes LTP (1). However, LTP and LTD can also be induced at the same stimulus frequency. This phenomenon has been demonstrated at hippocampal, neocortical, and cerebellar synapses, where potentiation and depression mechanisms operate over a wide range of activation frequencies (2-7). In the neocortex and hippocampus, the level of postsynaptic depolarization determines whether LTP or LTD results from stimulation at a given frequency (2, 5). These voltage-dependent thresholds for LTP and LTD induction reflect thresholds in calcium signal amplitudes (3,4,(8)(9)(10)(11)) that, when maintained for sufficiently long time periods (12), control synaptic plasticity in concert with distinct calcium sensors that are restricted to local microenvironments (13,14).At cerebellar parallel fiber (PF)-Purkinje cell synapses, both LTP and LTD can be induced using 1-Hz and 100-Hz PF stimulation protocols, ...

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Synaptic Activity Modulates the Induction of Bidirectional Synaptic Changes in Adult Mouse Hippocampus

Cited by 131 publications

References 54 publications

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

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

Calcium control of triphasic hippocampal STDP

Calcium threshold shift enables frequency-independent control of plasticity by an instructive signal

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