Experimental demonstration of short and long term synaptic plasticity using OxRAM multi k-bit arrays for reliable detection in highly noisy input data

2016 ◽  
Author(s):  
T. Werner ◽  
E. Vianello ◽  
O. Bichler ◽  
A. Grossi ◽  
E. Nowak ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Input Data ◽  
Experimental Demonstration ◽  
Noisy Input ◽  
Reliable Detection ◽  
Short And Long Term

scholarly journals Intracellular Ca2+ Release and Synaptic Plasticity: A Tale of Many Stores

2018 ◽  
Vol 25 (3) ◽  
pp. 208-226 ◽  
Author(s):  
Zahid Padamsey ◽  
William J. Foster ◽  
Nigel J. Emptage
Keyword(s):  
Endoplasmic Reticulum ◽  
Synaptic Plasticity ◽  
Synaptic Function ◽  
Intracellular Organelles ◽  
Short And Long Term ◽  
Central Synapses ◽  
Neural Signaling ◽  
Temporal Extent

Ca2+ is an essential trigger for most forms of synaptic plasticity. Ca2+ signaling occurs not only by Ca2+ entry via plasma membrane channels but also via Ca2+ signals generated by intracellular organelles. These organelles, by dynamically regulating the spatial and temporal extent of Ca2+ elevations within neurons, play a pivotal role in determining the downstream consequences of neural signaling on synaptic function. Here, we review the role of three major intracellular stores: the endoplasmic reticulum, mitochondria, and acidic Ca2+ stores, such as lysosomes, in neuronal Ca2+ signaling and plasticity. We provide a comprehensive account of how Ca2+ release from these stores regulates short- and long-term plasticity at the pre- and postsynaptic terminals of central synapses.

scholarly journals Author Correction: The FAAH inhibitor URB597 suppresses hippocampal maximal dentate afterdischarges and restores seizure-induced impairment of short and long-term synaptic plasticity

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Roberto Colangeli ◽  
Massimo Pierucci ◽  
Arcangelo Benigno ◽  
Giuseppe Campiani ◽  
Stefania Butini ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Short And Long Term

scholarly journals Role of RIM1α in short- and long-term synaptic plasticity at cerebellar parallel fibres

2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Michael Kintscher ◽  
Christian Wozny ◽  
Friedrich W. Johenning ◽  
Dietmar Schmitz ◽  
Jörg Breustedt
Keyword(s):  
Synaptic Plasticity ◽  
Parallel Fibres ◽  
Short And Long Term

scholarly journals Short-term depression and long-term plasticity together tune sensitive range of synaptic plasticity

2019 ◽  
Author(s):  
Nicolas Deperrois ◽  
Michael Graupner
Keyword(s):  
Synaptic Plasticity ◽  
Firing Rate ◽  
Somatosensory Cortex ◽  
Calcium Transients ◽  
Synaptic Efficacy ◽  
Short Term ◽  
Firing Rates ◽  
Short And Long Term ◽  
Activity Dependent

AbstractSynaptic efficacy is subjected to activity-dependent changes on short- and long time scales. While short-term changes decay over minutes, long-term modifications last from hours up to a lifetime and are thought to constitute the basis of learning and memory. Both plasticity mechanisms have been studied extensively but how their interaction shapes synaptic dynamics is little known. To investigate how both short- and long-term plasticity together control the induction of synaptic depression and potentiation, we used numerical simulations and mathematical analysis of a calcium-based model, where pre- and postsynaptic activity induces calcium transients driving synaptic long-term plasticity. We found that the model implementing known synaptic short-term dynamics in the calcium transients can be successfully fitted to long-term plasticity data obtained in visual- and somatosensory cortex. Interestingly, the impact of spike-timing and firing rate changes on plasticity occurs in the prevalent firing rate range, which is different in both cortical areas considered here. Our findings suggest that short- and long-term plasticity are together tuned to adapt plasticity to area-specific activity statistics such as firing rates.Author summarySynaptic long-term plasticity, the long-lasting change in efficacy of connections between neurons, is believed to underlie learning and memory. Synapses furthermore change their efficacy reversibly in an activity-dependent manner on the subsecond time scale, referred to as short-term plasticity. It is not known how both synaptic plasticity mechanisms – long- and short-term – interact during activity epochs. To address this question, we used a biologically-inspired plasticity model in which calcium drives changes in synaptic efficacy. We applied the model to plasticity data from visual- and somatosensory cortex and found that synaptic changes occur in very different firing rate ranges, which correspond to the prevalent firing rates in both structures. Our results suggest that short- and long-term plasticity act in a well concerted fashion.

scholarly journals Endocannabinoid dynamics gate spike-timing dependent depression and potentiation

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Yihui Cui ◽  
Ilya Prokin ◽  
Hao Xu ◽  
Bruno Delord ◽  
Stephane Genet ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Cellular Mechanism ◽  
Spike Timing ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Short And Long Term

Synaptic plasticity is a cardinal cellular mechanism for learning and memory. The endocannabinoid (eCB) system has emerged as a pivotal pathway for synaptic plasticity because of its widely characterized ability to depress synaptic transmission on short- and long-term scales. Recent reports indicate that eCBs also mediate potentiation of the synapse. However, it is not known how eCB signaling may support bidirectionality. Here, we combined electrophysiology experiments with mathematical modeling to question the mechanisms of eCB bidirectionality in spike-timing dependent plasticity (STDP) at corticostriatal synapses. We demonstrate that STDP outcome is controlled by eCB levels and dynamics: prolonged and moderate levels of eCB lead to eCB-mediated long-term depression (eCB-tLTD) while short and large eCB transients produce eCB-mediated long-term potentiation (eCB-tLTP). Moreover, we show that eCB-tLTD requires active calcineurin whereas eCB-tLTP necessitates the activity of presynaptic PKA. Therefore, just like glutamate or GABA, eCB form a bidirectional system to encode learning and memory.

A model synapse that incorporates the properties of short- and long-term synaptic plasticity

2003 ◽  
Vol 16 (8) ◽  
pp. 1161-1177 ◽  
Author(s):  
Armen R Sargsyan ◽  
Albert A Melkonyan ◽  
Costas Papatheodoropoulos ◽  
Hovhannes H Mkrtchian ◽  
George K Kostopoulos
Keyword(s):  
Synaptic Plasticity ◽  
Short And Long Term

scholarly journals Author Correction: The FAAH inhibitor URB597 suppresses hippocampal maximal dentate afterdischarges and restores seizure-induced impairment of short and long-term synaptic plasticity

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Roberto Colangeli ◽  
Massimo Pierucci ◽  
Arcangelo Benigno ◽  
Giuseppe Campiani ◽  
Stefania Butini ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Short And Long Term

Differing Mechanisms of Expression for Short- and Long-Term Potentiation

1997 ◽  
Vol 78 (1) ◽  
pp. 321-334 ◽  
Author(s):  
Paul E. Schulz ◽  
Jill C. Fitzgibbons
Keyword(s):  
Synaptic Plasticity ◽  
Extracellular Recording ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Induction Step ◽  
Term Potentiation ◽  
Short And Long Term

Schulz, Paul E. and Jill C. Fitzgibbons. Differing mechanisms of expression for short- and long-term potentiation. J. Neurophysiol. 78: 321–334, 1997. Long-term potentiation (LTP) is a use-dependent form of synaptic plasticity that is of great interest as a cellular mechanism that may contribute to memory storage. It is the sustained phase of population excitatory postsynaptic potential induced by high-frequency stimulation (HFS). HFS can also induce short-term potentiation (STP), a decremental potentiation lasting ∼15 min. It has been unclear whether STP is simply a reversible form of LTP elicited by subthreshold stimuli or whether it is an independently expressed form of synaptic plasticity. We have attempted to clarify the relationship between LTP and STP in the extracellular recording technique in area CA1 of the adult rat hippocampal slice preparation to test four predictions of the hypothesis that LTP and STP are expressed via the same mechanism. First, occluding LTP expression should block STP expression. Saturating LTP under six different conditions, however, did not occlude STP expression. Second, occluding STP expression should occlude LTP expression. The partial or full occlusion of STP by two maneuvers (increasing the stimulus intensity used for HFS or applying 3-isobutyl-1-methylxanthine), however, did not occlude LTP expression. Third, LTP increases and decreases paired-pulse facilitation (PPF), and STP should have the same effect. STP did not change PPF, however. The first three results, then, suggest that STP and LTP are expressed via different mechanisms. Fourth, STP should be maximal near the LTP induction threshold, and then decrease above it. Surprisingly, STP was maximal at or very close to the LTP induction threshold, but it did not decrease above this threshold. This relationship suggests the possibility that STP and LTP share an induction step(s). What is the function of the independently expressed STP? We find that LTP can be induced by two HFSs, each of which is subthreshold for LTP, if the second is given during STP from the first. This suggests that STP can temporarily lower the LTP induction threshold. Three lines of evidence, then, suggest that STP and LTP may be expressed via different mechanisms; however, the proximity of STP saturation to LTP induction suggests that they may share an induction step(s). STP may also have the very important function of temporarily lowering the LTP induction threshold. Finally, these data suggestion caution in interpreting LTP data obtained <20–30 min after HFS, because they may be contaminated by STP, which appears to have different underlying mechanisms.

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