Cooperativity between hippocampal–prefrontal short-term plasticity through associative long-term potentiation

2006 ◽  
Vol 1109 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Hitoshi Kawashima ◽  
Yoshinori Izaki ◽  
Anthony A. Grace ◽  
Masatoshi Takita
Keyword(s):  
Long Term Potentiation ◽  
Short Term ◽  
Short Term Plasticity ◽  
Term Potentiation

Short-term plasticity and long-term potentiation mimicked in single inorganic synapses

2011 ◽  
Vol 10 (8) ◽  
pp. 591-595 ◽  
Author(s):  
Takeo Ohno ◽  
Tsuyoshi Hasegawa ◽  
Tohru Tsuruoka ◽  
Kazuya Terabe ◽  
James K. Gimzewski ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Short Term ◽  
Short Term Plasticity ◽  
Term Potentiation

scholarly journals Phosphorylation-State-Dependent Regulation of NMDA Receptor Short-Term Plasticity Modifies Hippocampal Dendritic Ca2+ Transients

2010 ◽  
Vol 104 (4) ◽  
pp. 2203-2213 ◽  
Author(s):  
Debika Chatterjea ◽  
Edaeni Hamid ◽  
John P. Leonard ◽  
Simon Alford
Keyword(s):  
Nmda Receptor ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Short Term ◽  
Short Term Plasticity ◽  
State Dependent ◽  
Term Potentiation ◽  
Protocol Enhancement

N-methyl-d-aspartate (NMDA) receptor-mediated currents are enhanced by phosphorylation. We have investigated effects of phosphorylation-dependent short-term plasticity of NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) on the induction of long-term depression (LTD). We confirmed in whole cell clamped CA1 pyramidal neurons that LTD is induced by pairing stimulus protocols. However, after serine-threonine phosphorylation was modified by postsynaptic introduction of a protein phosphatase-1 (PP1) inhibitor, the same pairing protocol evoked long-term potentiation (LTP). We determined effects of modification of phosphatase activity on evoked NMDA EPSCs during LTD induction protocols. During LTD induction, using a protocol pairing depolarization to –40 mV and 0.5 Hz stimulation, NMDA receptor-mediated EPSCs undergo a short-term enhancement at the start of the protocol. In neurons in which PP1 activity was inhibited, this short-term enhancement was markedly amplified. We then investigated the effect of this enhancement on Ca2+ entry during the start of the LTD induction protocol. Enhancement of NMDA receptor-mediated responses was accompanied by an amplification of induction protocol-evoked Ca2+ transients. Furthermore, this amplification required synaptic activation during the protocol, consistent with an enhancement of Ca2+ entry mediated by NMDA receptor activation. The sign of NMDA receptor-mediated long-term plasticity, whether potentiation or depression depends on the amplitude of the synaptic Ca2+ transient during induction. We conclude that short-term phosphorylation-dependent plasticity of the NMDA receptor-mediated EPSCs contributes significantly to the effect of phosphatase inhibition on the subsequent induction of LTD or LTP.

Distinct Transmitter Release Properties Determine Differences in Short-Term Plasticity at Functional and Silent Synapses

2006 ◽  
Vol 95 (5) ◽  
pp. 3024-3034 ◽  
Author(s):  
Carolina Cabezas ◽  
Washington Buño
Keyword(s):  
Transmitter Release ◽  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Lower Percentage ◽  
Functional Importance ◽  
Short Term ◽  
Short Term Plasticity ◽  
Silent Synapses ◽  
Term Potentiation

Recent evidence suggests that functional and silent synapses are not only postsynaptically different but also presynaptically distinct. The presynaptic differences may be of functional importance in memory formation because a proposed mechanism for long-term potentiation is the conversion of silent synapses into functional ones. However, there is little direct experimentally evidence of these differences. We have investigated the transmitter release properties of functional and silent Schaffer collateral synapses and show that on the average functional synapses displayed a lower percentage of failures and higher excitatory postsynaptic current (EPSC) amplitudes than silent synapses at +60 mV. Moreover, functional but not silent synapses show paired-pulse facilitation (PPF) at +60 mV and thus presynaptic short-term plasticity will be distinct in the two types of synapse. We examined whether intraterminal endoplasmic reticulum Ca2+ stores influenced the release properties of these synapses. Ryanodine (100 μM) and thapsigargin (1 μM) increased the percentage of failures and decreased both the EPSC amplitude and PPF in functional synapses. Caffeine (10 mM) had the opposite effects. In contrast, silent synapses were insensitive to both ryanodine and caffeine. Hence we have identified differences in the release properties of functional and silent synapses, suggesting that synaptic terminals of functional synapses express regulatory molecular mechanisms that are absent in silent synapses.

Implementation of Short-Term Plasticity and Long-Term Potentiation in a Synapse Using Si-Based Type of Charge-Trap Memory

2015 ◽  
Vol 62 (2) ◽  
pp. 569-573 ◽  
Author(s):  
Myoung-Sun Lee ◽  
Ju-Wan Lee ◽  
Change-Hee Kim ◽  
Byung-Gook Park ◽  
Jong-Ho Lee
Keyword(s):  
Long Term Potentiation ◽  
Short Term ◽  
Charge Trap ◽  
Short Term Plasticity ◽  
Term Potentiation

Artificial Synaptic Behavior of Aloe Polysaccharides-Based Device with Au as Top Electrode

MRS Advances ◽  
2019 ◽  
Vol 5 (14-15) ◽  
pp. 693-698
Author(s):  
Z. X. Lim ◽  
I. A. Tayeb ◽  
Z. A. A. Hamid ◽  
M. F. Ain ◽  
A. M. Hashim ◽  
...  
Keyword(s):  
Metal Structure ◽  
Long Term Potentiation ◽  
Short Term ◽  
Short Term Plasticity ◽  
Voltage Sweep ◽  
Artificial Synapse ◽  
Term Potentiation ◽  
Metal Insulator Metal ◽  
Post Tetanic Potentiation

ABSTRACTFormulated, processed, and dried Aloe polysaccharides thin film sandwiched between ITO as bottom electrode and Au as top electrode has been adopted as an artificial synapse to emulate behavior of neuromorphic computing. The synaptic plasticity or weight has been modulated with this simple metal-insulator-metal structure by applying voltage sweep and voltage pulse, with excitatory postsynaptic current being monitored. Synaptic potentiation and depression has been demonstrated by applying 6 consecutive sweeps of voltage in positive and negative polarity, respectively. By varying number (10 – 50) of voltage pulses, variable synaptic weight has been measured with paired pulse facilitation and post-tetanic potentiation indexes of 2.61x10-6and 1.45x10-4, respectively. The short-term plasticity and long-term potentiation can be clearly revealed when applying 40 pulses and beyond, with extracted time constants of approximately 28 s at 40 pulses and 90 s at 50 pulses.

scholarly journals Multiplexed neurochemical transmission emulated using a dual-excitatory synaptic transistor

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Mingxue Ma ◽  
Yao Ni ◽  
Zirong Chi ◽  
Wanqing Meng ◽  
Haiyang Yu ◽  
...  
Keyword(s):  
Neural Network ◽  
Central Nervous System ◽  
Nervous System ◽  
Long Term Potentiation ◽  
Short Term ◽  
Term Potentiation ◽  
Binary Neural Network ◽  
Neuromorphic Systems ◽  
Human Brains

AbstractThe ability to emulate multiplexed neurochemical transmission is an important step toward mimicking complex brain activities. Glutamate and dopamine are neurotransmitters that regulate thinking and impulse signals independently or synergistically. However, emulation of such simultaneous neurotransmission is still challenging. Here we report design and fabrication of synaptic transistor that emulates multiplexed neurochemical transmission of glutamate and dopamine. The device can perform glutamate-induced long-term potentiation, dopamine-induced short-term potentiation, or co-release-induced depression under particular stimulus patterns. More importantly, a balanced ternary system that uses our ambipolar synaptic device backtrack input ‘true’, ‘false’ and ‘unknown’ logic signals; this process is more similar to the information processing in human brains than a traditional binary neural network. This work provides new insight for neuromorphic systems to establish new principles to reproduce the complexity of a mammalian central nervous system from simple basic units.

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