INT197375

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Context Info
Confidence 0.65
First Reported 2006
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 84
Total Number 85
Disease Relevance 16.46
Pain Relevance 16.45

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

lyase activity (Car1) Golgi apparatus (Car1) cytoplasm (Car1)
Anatomy Link Frequency
synapses 19
neurons 10
hippocampus 8
pyramidal neurons 6
dentate gyrus 4
Car1 (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 1883 100.00 Very High Very High Very High
Hippocampus 1288 100.00 Very High Very High Very High
Pyramidal cell 601 100.00 Very High Very High Very High
nMDA receptor 598 100.00 Very High Very High Very High
depression 328 99.68 Very High Very High Very High
amygdala 145 99.54 Very High Very High Very High
cerebral cortex 66 99.52 Very High Very High Very High
Nucleus accumbens 32 96.64 Very High Very High Very High
ischemia 70 96.12 Very High Very High Very High
adenocard 16 95.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 1148 99.72 Very High Very High Very High
Depression 372 99.68 Very High Very High Very High
Neurodegenerative Disease 397 99.58 Very High Very High Very High
Stress Fractures 53 98.88 Very High Very High Very High
Sprains And Strains 116 98.28 Very High Very High Very High
Schizophrenia 49 98.28 Very High Very High Very High
Cv Unclassified Under Development 62 96.12 Very High Very High Very High
Gliosis 46 95.12 Very High Very High Very High
Anxiety Disorder 684 93.44 High High
Congenital Anomalies 115 93.32 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The observed interaction between a CTR minor allele and the VDR C-A haplotype and their association with stress fractures may be explained by the inhibitory effect of these proteins on parathyroid hormone production.
Gene_expression (haplotype) of C-A in parathyroid associated with stress fractures
1) Confidence 0.65 Published 2010 Journal BMC Genet Section Body Doc Link PMC2975640 Disease Relevance 0.35 Pain Relevance 0
In particular, disruption of Hebbian plasticity at CA1 synapses in the hippocampus appears to interfere with NMDAR-dependent memory formation.


Gene_expression (synapses) of CA1 in hippocampus associated with hippocampus
2) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0 Pain Relevance 0.20
In addition, as predicted by our results showing that injected IL-6 induces brain Nox2, and that IL-6-/- mice lack induction of Nox2, there was preservation of these interneurons in aged IL-6-/- mice which was highly significant for CA3, and approached significance for CA1.
Gene_expression (approached) of CA1 in interneurons
3) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.42 Pain Relevance 0.13
The relative expression levels of the mRNAs in the hippocampal CA3 region were calculated using the ratio of the density in the CA3 region to that of the CA1 region, except that the GluR?
Gene_expression (region) of CA1
4) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2615205 Disease Relevance 0 Pain Relevance 0
Hence, NMDA receptors in the CA1 region are not considered to be involved in spontaneous network activity.
Gene_expression (receptors) of CA1 associated with nmda receptor
5) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2615205 Disease Relevance 0.07 Pain Relevance 0.61
A large body of evidence indicates the NMDAR is essential for a prominent form of synaptic plasticity, long-term potentiation (LTP) at Schaffer collateral-CA1 synapses, and for hippocampal-dependent spatial learning and memory [2,3].
Gene_expression (synapses) of CA1 in synapses associated with long-term potentiation
6) Confidence 0.40 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0 Pain Relevance 0.22
The reduction in tbLTP and NMDAR EPSCs at Schaffer collateral-CA1 synapses suggested that there might be a decrease in the abundance or function of synaptic NMDARs.
Gene_expression (synapses) of CA1 in synapses
7) Confidence 0.40 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.08 Pain Relevance 0.04
tbLTP at Schaffer collateral-CA1 synapses is NMDAR-dependent [31].
Gene_expression (synapses) of CA1 in synapses
8) Confidence 0.40 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0 Pain Relevance 0.12
In NR2A-null mutant mice, as in Neto1-null mice, LTP at Schaffer collateral-CA1 synapses is mediated by NR2B-NMDARs [54].
Gene_expression (synapses) of CA1 in synapses associated with long-term potentiation
9) Confidence 0.40 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0 Pain Relevance 0.10
These findings indicate that Neto1 plays a critical role in maintaining the delivery or stability of NR2A-containing NMDARs at CA1 synapses.
Gene_expression (synapses) of CA1 in synapses
10) Confidence 0.40 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0 Pain Relevance 0.06
To determine whether the decreased synaptic abundance of NR2A subunits leads to a reduction in NR2A-mediated synaptic currents we examined the relative contribution of NR2A versus NR2B to NMDAR EPSCs at CA1 synapses.
Gene_expression (synapses) of CA1 in synapses
11) Confidence 0.40 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0 Pain Relevance 0.16
The number of Nissl-stained neuronal profile in areas CA3, CA1, the dentate hilus, and the dentate gyrus were counted in both the right and left hippocampus in horizontal sections for each animal by using four to five Nissl-stained sections that were ?
Gene_expression (counted) of CA1 in hilus associated with hippocampus
12) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001489 Disease Relevance 0 Pain Relevance 0.13
Type-1 and type-2 interneurons were CA1 basket cells and bistratified cells according the characteristics of these cells [34], [35], [46] were made of nearly half of recorded interneurons.
Gene_expression (basket cells) of CA1 in interneurons
13) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2999569 Disease Relevance 0 Pain Relevance 0.38
Most native AMPA receptors consist of GluR2 plus GluR1 or GluR3 subunits in CA3-CA1 synapses.
Gene_expression (synapses) of CA1 in synapses
14) Confidence 0.37 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2169299 Disease Relevance 0.33 Pain Relevance 0.31
Our results demonstrate that deletion of GluR2 in the CA1 region of the hippocampus produces AMPAR-mediated plasticity that impairs learning and memory.
Gene_expression (region) of CA1 in hippocampus associated with hippocampus
15) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.30 Pain Relevance 0.13
Our electrophysiological data indicate that Ca2+-permeable AMPARs are present in the CA1 region of our GluR2-cKO mice and are able to mediate LTP in the absence of NMDAR activation.
Gene_expression (region) of CA1 associated with long-term potentiation
16) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0 Pain Relevance 0.08
This suggests that GluR2 deletion in CA1 selectively impairs NMDAR-dependent learning.
Gene_expression (deletion) of CA1
17) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0 Pain Relevance 0.18
These data suggest that deletion of GluR2 in the CA1 region of the hippocampus impairs the formation of spatial memory.
Gene_expression (region) of CA1 in hippocampus associated with hippocampus
18) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.11 Pain Relevance 0.14
Mutant mice were engineered with a conditional genetic deletion of GluR2 in the CA1 region of the hippocampus (GluR2-cKO mice).
Gene_expression (region) of CA1 in hippocampus associated with hippocampus
19) Confidence 0.37 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2947514 Disease Relevance 0.06 Pain Relevance 0.26
The induction of LTP by a conventional high-frequency stimulation (HFS) protocol was significantly enhanced in the CA1 region of GluR2-cKO mice (60 minutes post-HFS, fEPSPs were potentiated to 255±19% of baseline in GluR2-cKO mice, n?
Gene_expression (region) of CA1 associated with long-term potentiation
20) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.14 Pain Relevance 0.33

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