LEARNING IN AN OSCILLATORY CORTICAL MODEL

Fractals ◽  
2003 ◽  
Vol 11 (supp01) ◽  
pp. 291-300
Author(s):  
SILVIA SCARPETTA ◽  
ZHAOPING LI ◽  
JOHN HERTZ

We study a model of generalized-Hebbian learning in asymmetric oscillatory neural networks modeling cortical areas such as hippocampus and olfactory cortex. The learning rule is based on the synaptic plasticity observed experimentally, in particular long-term potentiation and long-term depression of the synaptic efficacies depending on the relative timing of the pre- and postsynaptic activities during learning. The learned memory or representational states can be encoded by both the amplitude and the phase patterns of the oscillating neural populations, enabling more efficient and robust information coding than in conventional models of associative memory or input representation. Depending on the class of nonlinearity of the activation function, the model can function as an associative memory for oscillatory patterns (nonlinearity of class II) or can generalize from or interpolate between the learned states, appropriate for the function of input representation (nonlinearity of class I). In the former case, simulations of the model exhibits a first order transition between the "disordered state" and the "ordered" memory state.

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Daniela Puzzo ◽  
Roberto Piacentini ◽  
Mauro Fá ◽  
Walter Gulisano ◽  
Domenica D Li Puma ◽  
...  

The concurrent application of subtoxic doses of soluble oligomeric forms of human amyloid-beta (oAβ) and Tau (oTau) proteins impairs memory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oligomers uptake. Intrigued by these findings, we investigated whether oAβ and oTau share a common mechanism when they impair memory and LTP in mice. We found that as already shown for oAβ, also oTau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oAβ and oTau requires expression of APP. Finally, the toxic effect of both extracellular oAβ and oTau on memory and LTP is dependent upon APP since APP-KO mice were resistant to oAβ- and oTau-induced defects in spatial/associative memory and LTP. Thus, APP might serve as a common therapeutic target against Alzheimer's Disease (AD) and a host of other neurodegenerative diseases characterized by abnormal levels of Aβ and/or Tau.


2019 ◽  
Vol 116 (13) ◽  
pp. 6397-6406 ◽  
Author(s):  
Xi Chen ◽  
Xiao Li ◽  
Yin Ting Wong ◽  
Xuejiao Zheng ◽  
Haitao Wang ◽  
...  

Memory is stored in neural networks via changes in synaptic strength mediated in part by NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). Here we show that a cholecystokinin (CCK)-B receptor (CCKBR) antagonist blocks high-frequency stimulation-induced neocortical LTP, whereas local infusion of CCK induces LTP. CCK−/−mice lacked neocortical LTP and showed deficits in a cue–cue associative learning paradigm; and administration of CCK rescued associative learning deficits. High-frequency stimulation-induced neocortical LTP was completely blocked by either the NMDAR antagonist or the CCKBR antagonist, while application of either NMDA or CCK induced LTP after low-frequency stimulation. In the presence of CCK, LTP was still induced even after blockade of NMDARs. Local application of NMDA induced the release of CCK in the neocortex. These findings suggest that NMDARs control the release of CCK, which enables neocortical LTP and the formation of cue–cue associative memory.


2004 ◽  
Vol 16 (3) ◽  
pp. 595-625 ◽  
Author(s):  
Ausra Saudargiene ◽  
Bernd Porr ◽  
Florentin Wörgötter

Spike-timing-dependent plasticity (STDP) is described by long-term potentiation (LTP), when a presynaptic event precedes a postsynaptic event, and by long-term depression (LTD), when the temporal order is reversed. In this article, we present a biophysical model of STDP based on a differential Hebbian learning rule (ISO learning). This rule correlates presynaptically the NMDA channel conductance with the derivative of the membrane potential at the synapse as the postsynaptic signal. The model is able to reproduce the generic STDP weight change characteristic. We find that (1) The actual shape of the weight change curve strongly depends on the NMDA channel characteristics and on the shape of the membrane potential at the synapse. (2) The typical antisymmetrical STDP curve (LTD and LTP) can become similar to a standard Hebbian characteristic (LTP only) without having to change the learning rule. This occurs if the membrane depolarization has a shallow onset and is long lasting. (3) It is known that the membrane potential varies along the dendrite as a result of the active or passive backpropagation of somatic spikes or because of local dendritic processes. As a consequence, our model predicts that learning properties will be different at different locations on the dendritic tree. In conclusion, such site-specific synaptic plasticity would provide a neuron with powerful learning capabilities.


2017 ◽  
Author(s):  
Zahid Padamsey ◽  
Rudi Tong ◽  
Nigel Emptage

AbstractLong-term potentiation (LTP) and long-term depression (LTD) of transmitter release probability (Pr) are thought to be triggered by the activation of glutamate receptors. Here, we demonstrate that glutamate release at CA3-CA1 synapses is in fact inhibitory and unnecessary for increases in Pr. Instead, at active presynaptic terminals, postsynaptic depolarization alone can increase Pr by promoting the release of nitric oxide from neuronal dendrites in a manner dependent on L-type voltage-gated Ca2+ channels. The release of glutamate, in contrast, decreases Pr by activating presynaptic NMDA receptors (NMDAR). Thus, net changes in Pr are determined by the combined effect of both LTP-promoting and LTD-promoting processes, that is, by the amount of glutamate release and postsynaptic depolarization that accompany presynaptic activity, respectively. Neither of these processes directly depends on the activation of postsynaptic NMDARs. We further show that presynaptic changes can be captured by a simple learning rule, in which the role of presynaptic plasticity is to ensure that the ability for a presynaptic terminal to release glutamate is matched with its ability to predict postsynaptic spiking.


1996 ◽  
Vol 76 (1) ◽  
pp. 631-636 ◽  
Author(s):  
D. V. Buonomano ◽  
M. M. Merzenich

1. Hebbian or associative synaptic plasticity has been proposed to play an important role in learning and memory. Whereas many behaviorally relevant stimuli are time-varying, most experimental and theoretical work on synaptic plasticity has focused on stimuli or induction protocols without temporal structure. Recent theoretical studies have suggested that associative plasticity sensitive to only the conjunction of pre- and postsynaptic activity is not an effective learning rule for networks required to learn time-varying stimuli. Our goal in the current experiment was to determine whether associative long-term potentiation (LTP) is sensitive to temporal structure. We examined whether the presentation of unpaired presynaptic pulses in addition to paired pre- and postsynaptic activity altered the induction of associative LTP. 2. By using intracellular recordings from CA1 pyramidal cells, associative long-term potentiation (LTP) was induced in a control pathway by pairing a single presynaptic pulse with postsynaptic depolarization every 5 s (50-70 x). The experimental pathway received the same training, with additional unpaired presynaptic pulses delivered in close temporal proximity, either after or before associative pairing. Five separate sets of experiments were performed with intervals of -200, -50, +50, +200, or +800 ms. Negative intervals indicate that the unpaired presynaptic pulse was presented before the depolarizing pulse. Our results showed that the presence of unpaired presynaptic pulses, occurring either before or after pairing, did not significantly alter the magnitude of LTP. 3. The experimental design permitted an analysis of whether changes in paired-pulse facilitation (PPF) occur as a result of associative LTP. The average degree of PPF was the same before and after LTP. However, there was a significant inverse correlation between the initial degree of PPF and the degree of PPF after LTP. There was no relationship between the change in PPF, and whether the first or second pulse had been paired with depolarization. 4. These results indicate that the presence of unpaired presynaptic pulses does not alter the induction of synaptic plasticity, suggesting that plasticity of the Schaffer collateral-CA1 synapse is primarily conjunctive rather than correlative.


2000 ◽  
Vol 20 (20) ◽  
pp. 7631-7639 ◽  
Author(s):  
Edda Thiels ◽  
Nathan N. Urban ◽  
Guillermo R. Gonzalez-Burgos ◽  
Beatriz I. Kanterewicz ◽  
German Barrionuevo ◽  
...  

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