INT7506

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Context Info
Confidence 0.46
First Reported 1983
Last Reported 2011
Negated 8
Speculated 6
Reported most in Body
Documents 267
Total Number 283
Disease Relevance 91.01
Pain Relevance 176.80

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

Anatomy Link Frequency
synapses 16
hippocampus 15
spinal 11
cortex 7
dentate gyrus 5
Ltp (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 8334 100.00 Very High Very High Very High
depression 2976 100.00 Very High Very High Very High
amygdala 2969 100.00 Very High Very High Very High
nMDA receptor 2363 100.00 Very High Very High Very High
Anterior cingulate cortex 1163 100.00 Very High Very High Very High
qutenza 959 100.00 Very High Very High Very High
c fibre 517 100.00 Very High Very High Very High
Pyramidal cell 468 100.00 Very High Very High Very High
Spinal cord 379 100.00 Very High Very High Very High
spinal dorsal horn 355 100.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
Depression 3172 100.00 Very High Very High Very High
Stress 1354 100.00 Very High Very High Very High
Pain 1057 100.00 Very High Very High Very High
Hyperalgesia 188 100.00 Very High Very High Very High
Multiple System Atrophy 9 100.00 Very High Very High Very High
Anorexia 4 100.00 Very High Very High Very High
Targeted Disruption 2650 99.86 Very High Very High Very High
Anaerobic Bacterial Infections 120 99.82 Very High Very High Very High
Death 160 99.76 Very High Very High Very High
Cv Unclassified Under Development 30 99.72 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The capsaicin-induced reduction of LTP was completely blocked by the nitric oxide synthase (NOS) inhibitor L-NAME and was absent in neuronal NOS as well as in TRPV1 deficient mice.
Negative_regulation (reduction) of LTP in neuronal associated with qutenza and long-term potentiation
1) Confidence 0.46 Published 2011 Journal PLoS ONE Section Abstract Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.60
It can be postulated that cannabinoid receptor activation does not directly inhibit the molecular mechanisms responsible for long-term synaptic plasticity, but instead impairs LTP by reducing presynaptic glutamate release.
Negative_regulation (impairs) of LTP associated with glutamate, cannabinoid receptor and long-term potentiation
2) Confidence 0.46 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.20
The deficient mechanisms causing lack of LTP in the 129S6/SvEvTac and DBA/2 appear to be at least partly different.
Negative_regulation (lack) of LTP
3) Confidence 0.45 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2409357 Disease Relevance 0.41 Pain Relevance 0.24
We tested whether LTP induced by the pairing protocol is prevented by postsynaptic application of a MAPK inhibitor, PD98059 [25] (Fig. 1C, D).
Spec (whether) Negative_regulation (prevented) of LTP associated with long-term potentiation
4) Confidence 0.43 Published 2007 Journal Mol Pain Section Body Doc Link PMC2245920 Disease Relevance 0 Pain Relevance 0.50
Considering that late-phase LTP was disrupted by application of protein synthesis inhibitors before and during LTP induction while their application after LTP induction had no effect on its maintenance [9], the late-phase LTP would be necessary for a transient but not persistent upregulation of protein synthesis.
Negative_regulation (disrupted) of LTP associated with long-term potentiation
5) Confidence 0.43 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.11 Pain Relevance 0.82
On the other hand, it is conceivable that CaMKIV is also involved in early-phase LTP, because our previous study has shown that early-phase LTP in the ACC, amygdala, insular cortex and somatosensory cortex was disrupted in CaMKIV knockout mice [19].
Negative_regulation (disrupted) of LTP in cortex associated with targeted disruption, somatosensory cortex, long-term potentiation, amygdala and anterior cingulate cortex
6) Confidence 0.43 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.33 Pain Relevance 0.76
Plasticity induced by HFS and TBS was entirely dependent on NMDA receptors, as incubation with a competitive NMDA receptor blocker completely abolished LTP (Figs, 6B, 7B).
Negative_regulation (abolished) of LTP associated with nmda receptor and long-term potentiation
7) Confidence 0.41 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1574331 Disease Relevance 0.06 Pain Relevance 0.46
The specific antagonist of cannabinoid receptor type 1 (CB1), AM 251, was also able to reduce the inhibitory effect of capsaicin on LA-LTP, suggesting that stimulation of TRPV1 provokes the generation of anandamide in the brain which seems to inhibit NO synthesis.
Negative_regulation (reduce) of LTP in brain associated with qutenza, cannabinoid receptor, antagonist, long-term potentiation and amygdala
8) Confidence 0.39 Published 2011 Journal PLoS ONE Section Abstract Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.62
Capsaicin dose-dependently reduces LA-LTP in horizontal slices
Negative_regulation (reduces) of LTP associated with qutenza, long-term potentiation and amygdala
9) Confidence 0.39 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.08
The capsaicin-induced reduction of LA-LTP could be also blocked by the specific TRPV1 antagonist AMG9810 (1 µM cap: 110.4±5.5% [n?
Negative_regulation (reduction) of LTP associated with qutenza, antagonist, long-term potentiation and amygdala
10) Confidence 0.39 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 1.76
Our results further show that capsaicin-induced suppression of HFS-induced LA-LTP is mediated by the stimulation of TRPV1 receptors, since capsazepine and AMG9810 blocked the capsaicin-induced effect and the effect was absent in TRPV1 deficient mice.
Negative_regulation (suppression) of LTP associated with qutenza, long-term potentiation and amygdala
11) Confidence 0.39 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0.32 Pain Relevance 1.65
In the amygdala, LTP induced by the pairing protocol is blockaded by NMDA receptor antagonist AP-5 [19].
Negative_regulation (blockaded) of LTP in amygdala associated with nmda receptor antagonist, long-term potentiation and amygdala
12) Confidence 0.38 Published 2009 Journal Mol Brain Section Body Doc Link PMC2644299 Disease Relevance 0 Pain Relevance 1.21
Further, our results showed that targeted mutation of the EphB1 receptor completely abolished the LTP in all mice tested (n = 9) (Fig. 5D).
Negative_regulation (abolished) of LTP associated with long-term potentiation
13) Confidence 0.37 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704201 Disease Relevance 0 Pain Relevance 0.45
Iontophoresis LTP was Ca2+ dependent, was blocked by MK-801, and occluded tetanus-induced LTP.
Negative_regulation (blocked) of LTP associated with anaerobic bacterial infections and long-term potentiation
14) Confidence 0.37 Published 1993 Journal Neuron Section Abstract Doc Link 8098611 Disease Relevance 0.10 Pain Relevance 0.66
We have previously shown that chronic concurrent nicotine treatment prevents stress-induced LTP impairment.
Negative_regulation (impairment) of LTP associated with stress, nicotine and long-term potentiation
15) Confidence 0.37 Published 2006 Journal Brain Res. Section Abstract Doc Link 16725127 Disease Relevance 0.66 Pain Relevance 0.58
However, acute nicotine treatment of rats (a single dose of 1 mg/kg; sc.) did not reverse chronic-stress-induced impairment of LTP.
Negative_regulation (impairment) of LTP associated with stress, nicotine and long-term potentiation
16) Confidence 0.37 Published 2006 Journal Brain Res. Section Abstract Doc Link 16725127 Disease Relevance 0.92 Pain Relevance 0.82
Herein, we investigated the effects of acute and chronic nicotine treatments on the chronic-stress-induced impairment of LTP in area CA1 of the hippocampus of urethane-anesthetized rats.
Negative_regulation (impairment) of LTP in hippocampus associated with stress, nicotine, hippocampus and long-term potentiation
17) Confidence 0.37 Published 2006 Journal Brain Res. Section Abstract Doc Link 16725127 Disease Relevance 0.87 Pain Relevance 0.74
This inhibition of LTP was blocked by IL-1beta tripeptide antagonist (Lys-D-Pro-Thr), suggesting that the inhibitory effect of mild ischemia on synaptic potentials and LTP may be mediated by the generation of IL-1beta.
Negative_regulation (inhibition) of LTP associated with ischemia, antagonist and long-term potentiation
18) Confidence 0.37 Published 1999 Journal Neurosci. Lett. Section Abstract Doc Link 10081976 Disease Relevance 1.09 Pain Relevance 0.70
Nicotine reduces stress-induced impairment of LTP, probably, through activation of nicotinic acetylcholine receptors in the hippocampus.
Negative_regulation (impairment) of LTP in hippocampus associated with stress, nicotine, hippocampus and long-term potentiation
19) Confidence 0.37 Published 2006 Journal Brain Res. Section Abstract Doc Link 16725127 Disease Relevance 0.72 Pain Relevance 0.60
Chronic but not acute nicotine treatment reverses stress-induced impairment of LTP in anesthetized rats.
Negative_regulation (impairment) of LTP associated with stress, anesthesia and nicotine
20) Confidence 0.37 Published 2006 Journal Brain Res. Section Title Doc Link 16725127 Disease Relevance 0.93 Pain Relevance 0.87

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