scholarly journals Postinduction Requirement of NMDA Receptor Activation for Late-Phase Long-Term Potentiation of Developing Retinotectal Synapses In Vivo

2011 ◽  
Vol 31 (9) ◽  
pp. 3328-3335 ◽  
Author(s):  
L.-q. Gong ◽  
L.-j. He ◽  
Z.-y. Dong ◽  
X.-h. Lu ◽  
M.-m. Poo ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Late Phase ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Term Potentiation ◽  
Nmda Receptor Activation

scholarly journals NMDA receptor activation induces long-term potentiation of glycine synapses

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222066 ◽  
Author(s):  
Michelle L. Kloc ◽  
Bruno Pradier ◽  
Anda M. Chirila ◽  
Julie A. Kauer
Keyword(s):  
Nmda Receptor ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Term Potentiation ◽  
Nmda Receptor Activation

Cell-Permeable Scavengers of Superoxide Prevent Long-Term Potentiation in Hippocampal Area CA1

1998 ◽  
Vol 80 (1) ◽  
pp. 452-457 ◽  
Author(s):  
Eric Klann
Keyword(s):  
Nmda Receptor ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Manganese Porphyrin ◽  
Area Ca1 ◽  
Term Potentiation ◽  
Hippocampal Area ◽  
Nmda Receptor Activation

Klann, Eric. Cell-permeable scavengers of superoxide prevent long-term potentiation in hippocampal area CA1. J. Neurophysiol. 80: 452–457, 1998. Long-term potentiation (LTP) in hippocampal area CA1 is generally dependent on N-methyl-d-aspartate (NMDA) receptor activation. Reactive oxygen species (ROS), including superoxide, are produced in response to NMDA receptor activation in a number of brain regions, including the hipppocampus. In this study, two cell-permeable manganese porphyrin compounds that mimic superoxide dismutase (SOD) were used to determine whether production of superoxide is required for the induction of LTP in area CA1 of rat hippocampal slices. Incubation of hippocampal slices with either Mn(III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) or Mn(III) tetrakis (1-methyl-4-pyridyl) porphyrin (MnTMPyP) prevented the induction of LTP. Incubation of slices with either light-inactivated MnTBAP or light-inactivated MnTMPyP had no effect on induction of LTP. Neither MnTBAP nor MnTMPyP was able to reverse preestablished LTP. These observations suggest that production of superoxide occurs in response to LTP-inducing stimulation and that superoxide is necessary for the induction of LTP.

scholarly journals Polygalasaponin F induces long-term potentiation in adult rat hippocampus via NMDA receptor activation

2012 ◽  
Vol 33 (4) ◽  
pp. 431-437 ◽  
Author(s):  
Feng Sun ◽  
Jian-dong Sun ◽  
Ning Han ◽  
Chuang-jun Li ◽  
Yu-he Yuan ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Rat Hippocampus ◽  
Adult Rat ◽  
Term Potentiation ◽  
Nmda Receptor Activation

scholarly journals Expression mechanisms underlying long-term potentiation: a postsynaptic view

2003 ◽  
Vol 358 (1432) ◽  
pp. 721-726 ◽  
Author(s):  
Roger A. Nicoll
Keyword(s):  
Nmda Receptor ◽  
Ampa Receptors ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Covalent Modification ◽  
Term Potentiation ◽  
Expression Mechanism

This review summarizes the various experiments that have been carried out to determine if the expression of long-term potentiation (LTP), in particular N -methyl-D-aspartate (NMDA) receptor-dependent LTP, is presynaptic or postsynaptic. Evidence for a presynaptic expression mechanism comes primarily from experiments reporting that glutamate overflow is increased during LTP and from experiments showing that the failure rate decreases during LTP. However, other experimental approaches, such as monitoring synaptic glutamate release by recording astrocytic glutamate transporter currents, have failed to detect any change in glutamate release during LTP. In addition, the discovery of silent synapses, in which LTP rapidly switches on α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function at NMDA-receptor-only synapses, provides a postsynaptic mechanism for the decrease in failures during LTP. It is argued that the preponderance of evidence favours a postsynaptic expression mechanism, whereby NMDA receptor activation results in the rapid recruitment of AMPA receptors as well as a covalent modification of synaptic AMPA receptors.

scholarly journals Temporal Profiling of Gene Networks Associated with the Late Phase of Long-Term Potentiation In Vivo

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40538 ◽  
Author(s):  
Margaret M. Ryan ◽  
Brigid Ryan ◽  
Madeleine Kyrke-Smith ◽  
Barbara Logan ◽  
Warren P. Tate ◽  
...  
Keyword(s):  
Gene Networks ◽  
Late Phase ◽  
Long Term Potentiation ◽  
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.

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