INT202868

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Context Info
Confidence 0.44
First Reported 2007
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 30
Total Number 31
Disease Relevance 15.48
Pain Relevance 7.42

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
neurons 5
dentate gyrus 4
cortex 2
bars 1
molecular layer 1
Car1 (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 275 100.00 Very High Very High Very High
Pyramidal cell 336 99.96 Very High Very High Very High
Hippocampus 603 99.36 Very High Very High Very High
ischemia 115 99.16 Very High Very High Very High
nMDA receptor 220 97.88 Very High Very High Very High
cINOD 183 97.40 Very High Very High Very High
Anterior cingulate cortex 38 94.08 High High
tetrodotoxin 5 92.80 High High
depression 35 91.96 High High
amygdala 35 91.60 High High
Disease Link Frequency Relevance Heat
Neurodegenerative Disease 916 100.00 Very High Very High Very High
Anaerobic Bacterial Infections 27 99.98 Very High Very High Very High
Sprains And Strains 145 99.76 Very High Very High Very High
Anxiety Disorder 195 99.40 Very High Very High Very High
Targeted Disruption 527 99.36 Very High Very High Very High
Cv Unclassified Under Development 84 99.16 Very High Very High Very High
Stroke 24 95.24 Very High Very High Very High
Gliosis 163 94.84 High High
Urological Neuroanatomy 15 94.52 High High
Repression 68 93.16 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results demonstrate that context fear conditioning produces normal activation of CA1 neurons in GluR2-cKO animals.
Positive_regulation (activation) of CA1 in neurons associated with anxiety disorder
1) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.53 Pain Relevance 0.10
This finding is consistent with recent data showing that NMDAR-dependent plasticity in CA1 is not required for the retention of spatial information across short intervals [46].
Neg (not) Positive_regulation (required) of CA1
2) Confidence 0.32 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.16 Pain Relevance 0.10
Within a mouse strain, carbachol-induced fast network oscillations in CA1 had the same frequency as oscillations in CA3.
Positive_regulation (induced) of CA1 associated with sprains and strains
3) Confidence 0.32 Published 2010 Journal Frontiers in Cellular Neuroscience Section Body Doc Link PMC2901093 Disease Relevance 0.25 Pain Relevance 0.38
Between mouse strains, oscillation frequency in CA1 showed similar differences as was the case for CA3 (NOD: 19.7?
Positive_regulation (frequency) of CA1 associated with sprains and strains
4) Confidence 0.32 Published 2010 Journal Frontiers in Cellular Neuroscience Section Body Doc Link PMC2901093 Disease Relevance 0.25 Pain Relevance 0.36
Phase coupling of gamma oscillations between CA1 and CA3 increases during memory retrieval (Montgomery and Buzsaki, 2007), which occurs at different gamma frequencies than between CA1 and the enthorinal cortex (Colgin et al., 2009).
Positive_regulation (increases) of CA1 in cortex
5) Confidence 0.29 Published 2010 Journal Frontiers in Cellular Neuroscience Section Body Doc Link PMC2901093 Disease Relevance 0.42 Pain Relevance 0.10
Electrophysiological analyses found that GluR2-cKO mice exhibit a novel form of LTP in CA1 that is mediated by Ca2+-permeable AMPARs and independent of NMDARs.
Neg (independent) Positive_regulation (independent) of CA1 associated with long-term potentiation
6) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.07 Pain Relevance 0.29
In our own MAPK/ERK studies, we found that learning about objects induces MAPK/ERK activation in the entorhinal cortex and dentate gyrus, while memory reactivation resulted in MAPK/ERK activation in entorhinal cortex and CA1, suggesting that cortico-hippocampal circuits engaged in consolidation and reconsolidation are at least in part distinct (Kelly et al., 2003).
Positive_regulation (activation) of CA1 in cortex
7) Confidence 0.27 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2992451 Disease Relevance 0.06 Pain Relevance 0.06
Then the electrode bundles were advanced slowly toward the hippocampal CA1 region, in daily increments of about 0.07 mm until the tips of the electrodes had reached the CA1, as deduced from an assessment of high-frequency ripples, field potential, and neuronal activity patterns [37], [39].
Positive_regulation (reached) of CA1 in neuronal
8) Confidence 0.27 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2999569 Disease Relevance 0.07 Pain Relevance 0.10
Chronic blockade of NMDA receptors in hippocampal slice cultures during the first two weeks of postnatal development leads to a substantial increase in synapse number and results in a more complex dendritic arborization of CA1 pyramidal cells [31].
Positive_regulation (increase) of CA1 in synapse associated with pyramidal cell and nmda receptor
9) Confidence 0.27 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2615205 Disease Relevance 0.17 Pain Relevance 0.56
Responses to CA1 hippocampal tetanic stimuli in WT and Cdk5 KO mice
Positive_regulation (stimuli) of CA1 associated with targeted disruption
10) Confidence 0.25 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2695674 Disease Relevance 1.10 Pain Relevance 0.20
Stimulation of the SC/CA1 pathway at 20%-maximal stimulation intensity produced population spikes in 3.7±2.5% of WT and 10.4±5.0% of KO slices.
Positive_regulation (Stimulation) of CA1 in spikes associated with targeted disruption
11) Confidence 0.25 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2695674 Disease Relevance 0.45 Pain Relevance 0.16
Conditional loss of Cdk5 leads to an enhancement in CA1 hippocampal post-tetanic potentiation
Positive_regulation (enhancement) of CA1
12) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2695674 Disease Relevance 0.79 Pain Relevance 0.17
We also detected higher LTP after tetanus stimulation in CA1 and dentate gyrus of anesthetized CS-KO mice (Huang and Saido, unpublished data).
Positive_regulation (stimulation) of CA1 in dentate gyrus associated with targeted disruption, anaerobic bacterial infections and long-term potentiation
13) Confidence 0.19 Published 2008 Journal Mol Brain Section Body Doc Link PMC2561015 Disease Relevance 1.07 Pain Relevance 0.18
However, despite a huge amount of literature on hippocampal LTP, it remains to be demonstrated that if a simple spatial training trial may induce LTP in certain population of CA1 neurons.
Positive_regulation (population) of CA1 in neurons associated with long-term potentiation
14) Confidence 0.18 Published 2009 Journal Mol Brain Section Body Doc Link PMC2644299 Disease Relevance 1.02 Pain Relevance 1.27
(25–35)-injected mice receiving vehicle compared to control mice, and administration of Kihi-to resulted in significant increases in P-NF-H expression levels in CA1 radiatum, dentate gyrus, parietal cortex, perirhinal cortex and the striatum (Figures 3 and 7).
Positive_regulation (increases) of CA1 in parietal cortex
15) Confidence 0.18 Published 2008 Journal BMC Complement Altern Med Section Body Doc Link PMC2532680 Disease Relevance 0.20 Pain Relevance 0.09
(25–35)-injected mice receiving vehicle, and administration of Kihi-to resulted in significant increases in synaptophysin expression levels in CA1, the oriens and radiatum in CA3, the molecular layer in dentate gyrus (Figures 5 and 7).
Positive_regulation (increases) of CA1 in molecular layer
16) Confidence 0.18 Published 2008 Journal BMC Complement Altern Med Section Body Doc Link PMC2532680 Disease Relevance 0.06 Pain Relevance 0
In the hippocampal CA1 region where most of LTP studies have been reported, LTP can be induced and reliable detected, even with field recording electrodes [7,8].
Positive_regulation (induced) of CA1 associated with long-term potentiation
17) Confidence 0.15 Published 2009 Journal Mol Brain Section Body Doc Link PMC2644299 Disease Relevance 0.81 Pain Relevance 1.09
Consistent with the role of activin A in regulating astrocyte proliferation after KA-induced neurodegeneration, infusion of FS-288 following KA injection resulted in a 94%, 187%, and 194% increase in the average number of proliferating astrocytes in the DG, CA3, and CA1 regions, respectively, but not in the neurogenic pPV, when compared to KA-injected animals that received no FS-288 (Fig. 3K).
Positive_regulation (increase) of CA1 in astrocytes
18) Confidence 0.15 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.37 Pain Relevance 0.19
Indeed, the average number of newly generated neurons in the DG, CA3, and CA1 was increased by 547%, 371%, and 299%, respectively, in animals that received NSAIDs compared to the DG, CA3, and CA1 regions of KA-injected (FS-288)-treated animals that did not receive NSAIDs (Fig. 7G).
Positive_regulation (increased) of CA1 in neurons associated with cinod
19) Confidence 0.15 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.96 Pain Relevance 0.55
As expected, there was a 96%, 65%, and 234% increase in the average number of newly generated neurons in the DG, CA3, or CA1 regions of the hippocampus of animals that received activin A, compared to animals that received no activin A after a PBS injection.
Positive_regulation (increase) of CA1 in neurons associated with hippocampus
20) Confidence 0.13 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.54 Pain Relevance 0.05

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