scholarly journals Developmental Exposure of Rats to a Reconstituted PCB Mixture or Aroclor 1254: Effects on Long-Term Potentiation and [3H]MK-801 Binding in Occipital Cortex and Hippocampus

2001 ◽  
Vol 61 (2) ◽  
pp. 321-330 ◽  
Author(s):  
L. Altmann
Keyword(s):  
Occipital Cortex ◽  
Long Term Potentiation ◽  
Aroclor 1254 ◽  
Developmental Exposure ◽  
Mk 801 ◽  
Term Potentiation

scholarly journals GluA1 trafficking and metabotropic NMDA: addressing results from other laboratories inconsistent with ours

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130145 ◽  
Author(s):  
Sadegh Nabavi ◽  
Rocky Fox ◽  
Stephanie Alfonso ◽  
Jonathan Aow ◽  
Roberto Malinow
Keyword(s):  
Fluorescent Protein ◽  
Long Term Potentiation ◽  
Long Term Depression ◽  
Mk 801 ◽  
Over Expression ◽  
Term Potentiation ◽  
The Difference ◽  
Green Fluorescent ◽  
Gfp Tag

We have previously shown that when over-expressed in neurons, green fluorescent protein (GFP) tagged GluA1 (GluA1-GFP) delivery into synapses is dependent on plasticity. A recent study suggests that GluA1 over-expression leads to its incorporation into the synapse, in the absence of additional long-term potentiation-like manipulations. It is possible that a GFP tag was responsible for the difference. Using rectification index as a measure of synaptic delivery of GluA1, we found no difference in the synaptic delivery of GluA1-GFP versus untagged GluA1. We recently published a study showing that while D-APV blocks NMDAr-dependent long-term depression (LTD), MK-801 and 7-chloro kynurenate (7CK) fail to block LTD. We propose a metabotropic function for the NMDA receptor in LTD induction. In contrast to our observations, recent unpublished data suggest that the above antagonists are equally effective in blocking LTD. We noticed different methodology in their study. Here, we show that their methodology has complex effects on synaptic transmission. Therefore, it is not possible to conclude that 7CK is effective in blocking LTD from their type of experiment.

Enhancement of long-term potentiation at CA1-subiculum synapses in MK-801-treated rats

2006 ◽  
Vol 392 (1-2) ◽  
pp. 5-9 ◽  
Author(s):  
Nadine Buck ◽  
Sebat Cali ◽  
Joachim Behr
Keyword(s):  
Long Term Potentiation ◽  
Mk 801 ◽  
Term Potentiation

Knockdown of α2C-adrenoceptors in the occipital cortex rescued long-term potentiation in hidden prenatally malnourished rats

2012 ◽  
Vol 98 (3) ◽  
pp. 228-234 ◽  
Author(s):  
Rafael Barra ◽  
Rubén Soto-Moyano ◽  
Luis Valladares ◽  
Carlos Morgan ◽  
Hernán Pérez ◽  
...  
Keyword(s):  
Occipital Cortex ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Differential effects of ketamine and MK-801 on the induction of long-term potentiation

Neuroreport ◽  
1991 ◽  
Vol 2 (5) ◽  
pp. 239-242 ◽  
Author(s):  
Stephen Maren ◽  
Michel Baudry ◽  
Richard F. Thompson
Keyword(s):  
Long Term Potentiation ◽  
Mk 801 ◽  
Differential Effects ◽  
Term Potentiation

scholarly journals Investigating Parietal and Premotor Influence on Motor Cortical Excitability Associated with Visuomotor Associative Plasticity

2021 ◽  
Vol 11 (4) ◽  
pp. 452
Author(s):  
Paul J. Wolfe ◽  
Lynea B. Kaethler ◽  
W. Richard Staines
Keyword(s):  
Repeated Measures ◽  
Cortical Excitability ◽  
Occipital Cortex ◽  
Long Term Potentiation ◽  
Future Research ◽  
Reaching Movement ◽  
Repeated Measures Design ◽  
Term Potentiation ◽  
Motor Cortex Excitability

The brain changes in response to sensory signals it is exposed to. It has been shown that long term potentiation-like neuroplasticity can be experimentally induced via visual paired-associative stimulation (V-PAS). V-PAS combines afferent visual stimuli with a transcranial magnetic stimulation pulse to induce plasticity. Preparation of a reaching movement to generate activity in superior parietal occipital cortex (SPOC) was used in this study as an additional afferent contributor to modulate the resultant plasticity. We hypothesized that V-PAS with a reaching movement would induce greater cortical excitability than V-PAS alone and would exhibit facilitated SPOC to M1 projections. All four experiments enrolled groups of 10 participants to complete variations of V-PAS in a repeated measures design. SPOC to M1 projections facilitated motor cortex excitability following V-PAS regardless of intervention received. We did not observe evidence indicating extra afferent information provided an additive effect to participants. Investigation of PMd to M1 projections confirmed disinhibition and suggested interneuronal populations within M1 may be mechanistically involved. Future research should look to rule out the existence of an upper limit for effective afference during V-PAS and investigate the average influence of V-PAS on cortical excitability in the larger population.

scholarly journals Blockade of Motor Cortical Long-Term Potentiation Induction by Glutamatergic Dysfunction Causes Abnormal Neurobehavior in an Experimental Subarachnoid Hemorrhage Model

2021 ◽  
Vol 15 ◽  
Author(s):  
Minoru Fujiki ◽  
Kazuhiro Kuga ◽  
Harushige Ozaki ◽  
Yukari Kawasaki ◽  
Hirotaka Fudaba
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Motor Evoked Potentials ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Functional Evaluation ◽  
Evaluation Tool ◽  
Mk 801 ◽  
Term Potentiation ◽  
Motor Cortical

Subarachnoid hemorrhage (SAH) is a life-threatening condition that can also lead to permanent paralysis. However, the mechanisms that underlying neurobehavioral deficits after SAH have not been fully elucidated. As theta burst stimulation (TBS) can induce long-term potentiation (LTP) in the motor cortex, we tested its potential as a functional evaluation tool after experimentally induced SAH. Motor cortical inter-neuronal excitability was evaluated in anesthetized rats after 200 Hz-quadripulse TBS (QTS5), 200 Hz-quadripulse stimulation (QPS5), and 400 Hz-octapulse stimulation (OPS2.5). Furthermore, correlation between motor cortical LTP and N-methyl-D-aspartate-receptor activation was evaluated using MK-801, a NMDA-receptor antagonist. We evaluated inhibition-facilitation configurations [interstimulus interval: 3 ms; short-latency intracortical inhibition (SICI) and 11 ms; intracortical facilitation (ICF)] with paired electrical stimulation protocols and the effect of TBS paradigm on continuous recording of motor-evoked potentials (MEPs) for quantitative parameters. SAH and MK-801 completely blocked ICF, while SICI was preserved. QTS5, QPS5, and OPS2.5 facilitated continuous MEPs, persisting for 180 min. Both SAH and MK-801 completely blocked MEP facilitations after QPS5 and OPS2.5, while MEP facilitations after QTS5 were preserved. Significant correlations were found among neurological scores and 3 ms-SICI rates, 11 ms-ICF rates, and MEP facilitation rates after 200 Hz-QTS5, 7 days after SAH (R2 = 0.6236; r = −0.79, R2 = 0.6053; r = −0.77 and R2 = 0.9071; r = 0.95, p < 0.05, respectively). Although these findings need to be verified in humans, our study demonstrates that the neurophysiological parameters 3 ms-SICI, 11 ms-ICF, and 200 Hz-QTS5-MEPs may be useful surrogate quantitative biomarkers for assessing inter-neuronal function after SAH.

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