Bliss TVP, Collingridge GL. 1993. A synaptic model of memory: longterm potentiation in hippocampus. Nature 361:31--39.  Home/Search   Document Not in Database   Summary   Related Articles   Check

....in the past years. 6.2. 1 Dependence on the post synaptic depolarization The most classical recipe to induce long term potentiation is the following: the post synaptic neuron is strongly depolarized and the pre synaptic neuron is injected a current to emit a high frequency burst (see e.g. [67]) The protocols for inducing LTD are more diverse and controversial but, again, they depend on how much the post synaptic neuron is depolarized (a good review can be found in [68] Here we introduce a proper dependence on the postsynaptic depolarization to achieve the scheme of modifications ....

T. V. P. Bliss, G. L. Collingridge, A synaptic model of memory: long term potentiation in the hippocampus, Nature 361 (1993) 31--39.

....w ij , i.e. u i = w ij # j . In the following we assume that the firing rates # i , # j of pre and postsynaptic neurons are constant during one trial of an experiment. For several classical experiments on long term potentiation (LTP) this is a reasonable assumption; see [Brown et al. 1989, Bliss and Collingridge, 1993] for a review. LTP can, for example, be introduced by high frequency trains of presynaptic pulses at several synapses that are maintained over a time . In such a situation the temporal resolution is rather coarse and a description of pre and postsynaptic activity by fixed rates is ....

Bliss, T. V. P. and Collingridge, G. L. (1993). A synaptic model of memory: long-term potentiation in the hippocampus. Nature, 361:31--39.

....paired activityinthe source and target neuron. Because of its Hebbian properties, long term potentiation has generated a great deal of interest in the neuroscience community. As a result, our understanding of the mechanisms underlying LTP is changing rapidly. A recent 123 review can be found in [5]. E.2.1 Stages in LTP induction and maintenance Like the forms of learning seen in Aplysia, long term potentiation has several stages, ranging from short term potentiation which lasts about an hour, through three different stages of long term potentiation, which depend on differenttypes of ....

T. V. P. Bliss and G. L. Collingridge. A synaptic model of memory: long-term potentiation in the hippocampus. Nature, 361, 1993.

....behaviors produce ranges of N I with few, discrete categories of OE i , while non locked ones produce a vertically dense distribution of points within a range of OE i . 3 Results Magnification ratios obtained from the LTP simulation, shown in Fig. 2, mimic those found in living preparations [3, 10, 5]. They increase continuously from their unpotentiated values to their asymptotic 2 25 30 35 40 45 50 55 60 65 70 75 0.5 0.6 0.7 0.8 0.9 1.1 1.2 1.3 1.4 1.5 x 10 7 time, sec) m s) N I = 1.0 N I = 0.5 N I = 1.5 Figure 2: Magnification Ratio versus simulation time for N=I = 0:5; ....

....PSP simulation with P syn;f = 5 Theta 10 cm s, LTP glutamate transmitter amount, A = 0:533, LTP decay time constant, ff = 1=223 msec and LTP growth rate, fl = 25. values which depend directly on presynaptic rate for pacemaker input. This has also been reported in other experiments [10]. This increase in synaptic permeability modifies the global behavior of the neuron. From the bifurcation diagrams in Fig. 3, one can see the increase in locked responses as a result of LTP. Without LTP enhancement, 62 of the neural responses were locked. However, with LTP, 84 of input rates in ....

T. Bliss and G. Collingridge, "A synaptic model of memory: Long-term potentiation in the hippocampus, " Nature, vol. 361, pp. 31--39, Jan. 1993. 4

....number of bindings associated with this event. This article partially describes a computational model, SMRITI, that demonstrates how a transient pattern of activity representing an event can lead to the rapid formation of appropriate functional units as a result of long term potentiation (LTP) [2] within structures whose architecture and circuitry match those of the HS. The model shows that the seemingly idiosyncratic architecture of the HS and the existence of different types of inhibitory interneurons, and different types of local inhibitory circuits in the HS, are ideally suited for the ....

....emotional, and motivational aspects of behavior. These inputs can communicate the affective significance of an experience stimulus to the HS. 1. 2 Long Term Potentiation LTP refers to long term activity dependent increase in synaptic strength and is believed to underlie memory formation [2]. In particular, convergent activity at multiple synapses that share the same postsynaptic cell can lead to their associative LTP. The proposed computational model uses a highly idealized, but computationally effective, form of associative LTP. In brief, the occurrence of LTP in the model is ....

T.V.P. Bliss and G.L. Collingridge, A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361 (1993) 31-39.

....stimulus, the highfrequency activity during the memorizing period (Fig. 1a) effects the redistribution of synaptic weights according to Hebbian learning rules: increases in weights simulate, for example, long term potentiation (LTP) and decreases simulate, for example, longterm depression (LTD) (Bliss and Collingridge, 1993; Ito, 1989) The redistribution of weights results in an increase in the magnitude of postsynaptic potentials produced by the first spikes evoked by a future occurrence of that stimulus. The consequent increase in neuronal firing during the familiarity discrimination period when a stimulus ....

....Decision neurons receive inputs from the FDNs and are activated only when a majority of their inputs are active. These decision neurons govern the subsequent activity of the network, particularly the activity that will produce changes in synaptic efficacy according to Hebbian learning (LTP or LTD) (Bliss and Collingridge, 1993; Ito, 1989) for novel but not familiar patterns. Essentially, these neurons act as enforcers of the network decision. These neurons could be regarded as the output of the network in that they carry its decision; however, the FDNs provide a signal that is more biologically useful for distribution ....

Bliss TVP, Collingridge GL (1993) A synaptic model of memory: Long-term potentiation in hippocampus. Nature 361:31--39.

....as a more likely effect of slip under the existing circumstances. 2.1. 6 Explaining away in the Causal Model A explaining away phenomena also occurs in the causal model as a result of inhibitory connections be 2 This is modeled after the biological phenomena of short term potentiation (STP) [2]. 300 200 100 0 100 80 60 40 20 0 :trips :slips Figure 2: The activation trace of collector nodes :slip and :trip during the processing of the John fell story. X axis records the number of cycles. Each cycle may correspond to 50 100 msecs. tween rules which share the same ....

Bliss, T.V.P. and Collingridge, G.L. (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361, 31--39.

....of a slip event. In these circumstances, it is highly likely that the fall event actually occurred and is both an effect of the slip event and an explanation of the fall event. SHRUTI expresses this increased likelihoodvia the biologicallyplausible mechanism of short term potentiation(STP) (Bliss and Collingridge, 1993). Whenever a collector :P receives activity from one of its T or E fact and concurrent activity from a mediator collector node, then the weights of the links from the mediator collector to :P and from the active T facts to :P increase for a short duration. Analogous short term weight changes ....

Bliss, T.V.P. and Collingridge, G.L. (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361, 31--39.

....2 Introduction Since its conception half a century ago, Hebbian learning has become a fundamental paradigm in the neurosciences. The idea that neurons that re together wire together has become fairly well understood, as in the case of NMDA dependent long term potentiation in the Hippocampus [2]. However, for both computational and biological reasons, this type of plasticity has to be accompanied by synaptic changes that are not synapse speci c but neuron speci c, i.e. they involve many synapses of the same neuron. Biologically, such interactions are inevitable as synapses compete for ....

T.V.P. Bliss and G.L. Collingridge. Synaptic model of memory: long-term potentiation in the hippocampus. Nature, 361:31-39, 1993.

....which allows more precise weight modifications and results in improved network performance. The proposed algorithm utilises the property of synaptic plasticity in the brain, i.e. that a higher intensity of activity is more likely to produce a higher magnitude of synaptic weight modification [3]. The error of the network during the initial classification period regulates the frequency of neuronal activity in the succeeding memorising period via an inhibitory circuit. This mechanism causes the magnitude of change of all synaptic weights in the network to be proportional to the network ....

....memorising period. The lower the number of active decision neurons (i.e. the higher the error) the lower the inhibition and hence the higher the neuronal activity (see Figure 3 for sample simulation results) Since the magnitude of weight modification depends on the frequency of activation (see [3]) higher error causes larger modification of FDNs weights. In the network the firing frequency of the FDNs carries information about the value of the error. However, here for simplicity this effect is not simulated explicitly. Instead, we use the term d in Equation 2, which regulates the ....

Bliss, T.V.P., & Collingridge, G.L. (1993). A synaptic model of memory: long-term potentiation in hippocampus. Nature, 361, 31-9.

....postulated that learning of cell assemblies might be provided by a synaptic strengthening between the neurons actively involved. For a long time these postulates could be neither confirmed nor refuted experimentally. More recently, Hebbian learning mechanisms have gained some experimental evidence [7, 10, 65], but an experimental proof for the existence of cell assemblies is still out of reach. Nonetheless, Hebb s postulates were extremely fruitful to theoretical brain research and opened the way to a new paradigm, the computational methapher of the brain. The early cybernetics approach, for example, ....

T.V.P. Bliss and G.L. Collingridge. A synaptic model of memory: long-term potentiation in the hippocampus. Nature, 361:31--39, 1993.

No context found.

Bliss TVP, Collingridge GL. 1993. A synaptic model of memory: longterm potentiation in hippocampus. Nature 361:31--39.

No context found.

Bliss TVP, Collingridge GL (1993) A synaptic model of memory: long-term potentiation in hippocampus. Nature 361: 31-39.

No context found.

T. V. Bliss and G. L. Collingridge, "A synaptic model of memory: Long-term potentiation in the hippocampus," Nature, vol. 361, pp. 31--39, 1993.

No context found.

T.V.P. Bliss and G.L. Collingridge. A synaptic model of memory; long-term potentiation the hippocampus. Nature, 361:31--9, 1993.

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T. V. P. Bliss and G. L. Collingridge. A synaptic model of memory: Long term potentiation in the hippocampus. Nature, 31:361, 1993.

No context found.

Bliss, T.V.P., & Collingridge, G.L. (1993). A synaptic model of memory: long-term potentiation in hippocampus. Nature, 361, 31-9.

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T. V. P. Bliss and G. L. Collingridge. A synaptic model of memory: Long term potentiation in the hippocampus. Nature, 31:361, 1993.

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TVP Bliss and GL Collingridge, A synaptic model of memory: long term potentiation in the hippocampus, Nature 361 (1993), 31--39.

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Bliss TVP, Collingridge GL (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361:31-39.

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Bliss, T.V.P., Collingridge, G.L.: A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361, #1993# 31#39.

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Bliss TVP, Collingridge GL (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361:31-39.

No context found.

Bliss, T.V. and Collingridge, G.L. (1993) A synaptic model of memory: long-term potentiation in the hippocampus Nature 361, 31--39

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Bliss, T.V.P. and G.L. Collingridge (1993). A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361, 31--39.

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Neurosci., 2:32--48. Bliss T. V. P., Collingridge G. L., 1993, A synaptic model of memory: long-term potentiation in the hippocampus. Nature, 361:31--39.

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