INT182574

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Context Info
Confidence 0.73
First Reported 2005
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 15
Disease Relevance 5.47
Pain Relevance 11.44

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

plasma membrane (Slc1a3)
Anatomy Link Frequency
brain 2
sciatic nerve 2
spinal cord 1
hippocampus 1
cerebellum 1
Slc1a3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate 1061 100.00 Very High Very High Very High
Hippocampus 6 99.84 Very High Very High Very High
spinal dorsal horn 73 99.68 Very High Very High Very High
Spinal cord 175 99.28 Very High Very High Very High
Sciatic nerve 54 99.24 Very High Very High Very High
Lasting pain 42 98.90 Very High Very High Very High
Thermal hyperalgesia 13 98.80 Very High Very High Very High
antinociception 30 98.76 Very High Very High Very High
ischemia 69 97.04 Very High Very High Very High
intrathecal 37 94.68 High High
Disease Link Frequency Relevance Heat
Pain 267 98.90 Very High Very High Very High
Hyperalgesia 14 98.80 Very High Very High Very High
Nervous System Injury 107 98.04 Very High Very High Very High
Brain Hemorrhage 15 97.04 Very High Very High Very High
Nociception 74 95.80 Very High Very High Very High
Cv Unclassified Under Development 51 89.88 High High
Neuropathic Pain 46 88.24 High High
Pathologic Processes 8 83.84 Quite High
Hypersensitivity 55 82.24 Quite High
Toxicity 4 80.08 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
EAAC1 is generally considered as a neuronal GT, whereas GLAST and GLT1 are primarily astroglial GT, although both GLAST and GLT1 also have been located in neuronal cells during the developmental stage [2,3].
Localization (located) of GLAST in developmental stage
1) Confidence 0.73 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074355 Disease Relevance 0.22 Pain Relevance 0.67
GLAST, and GLT-1 are predominantly localized in astrocytes [2,20,21], while EAAC-1, EAAT4, and EAAT5 appears to be mostly neuronal [22-25].
Localization (localized) of GLAST in neuronal
2) Confidence 0.68 Published 2007 Journal Mol Pain Section Body Doc Link PMC1864984 Disease Relevance 0.60 Pain Relevance 1.02
This conclusion is consistent with reports on the distribution of GLT-1 and GLAST in hippocampus and cerebellum where the transporters were found to be in astrocytes [18-21].
Localization (distribution) of GLAST in cerebellum associated with hippocampus
3) Confidence 0.60 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.15 Pain Relevance 0.28
This issue was explored in this study by examination of changes in the expression and cellular localization of GLT-1 and GLAST in the spinal dorsal horn over time following partial sciatic nerve ligation (PNSL).


Localization (localization) of GLAST in sciatic nerve associated with spinal dorsal horn and sciatic nerve
4) Confidence 0.56 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.49 Pain Relevance 0.63
The results of this study demonstrate plasticity not only in the expression levels but also in the cellular localization of the glutamate transporters GLT-1 and GLAST following partial sciatic nerve ligation.
Localization (localization) of GLAST in sciatic nerve associated with glutamate and sciatic nerve
5) Confidence 0.56 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.17 Pain Relevance 0.25
GLT-1 and GLAST were not co-localized with the microglia marker OX-42 or the neuron marker NeuN at baseline, but rather only in cells positive for the astrocyte marker GFAP.
Localization (localized) of GLAST in astrocyte
6) Confidence 0.56 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.12 Pain Relevance 0.26
acid transporters: EAAT1 (GLAST), EAAT2 (GLT-1), EAAT3 (EAAC1),
Localization (transporters) of EAAT1
7) Confidence 0.53 Published 2007 Journal Experimental Diabetes Research Section Body Doc Link PMC1940058 Disease Relevance 0.05 Pain Relevance 0.53
As noted above, there was no co-localization of GLT-1 or GLAST with OX-42 positive microglia in the absence of nerve injury.
Localization (localization) of GLAST in nerve associated with nervous system injury
8) Confidence 0.49 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.31 Pain Relevance 0.07
For example, during brain ischemia, ATP is depleted and impairment of Na+-K+ATPase results in the increases in intracellular Na+ ions and extracellular K+ ions, which causes inverse operation of the glutamate transporter and release of glutamate into the extracellular space [3].
Localization (release) of glutamate transporter in brain associated with brain hemorrhage, glutamate and ischemia
9) Confidence 0.48 Published 2005 Journal Mol Pain Section Body Doc Link PMC1274343 Disease Relevance 0.39 Pain Relevance 1.08
For example, during brain ischemia, ATP is depleted and impairment of Na+-K+ATPase results in the increases in intracellular Na+ ions and extracellular K+ ions, which causes inverse operation of the glutamate transporter and release of glutamate into the extracellular space [3].
Localization (operation) of glutamate transporter in brain associated with brain hemorrhage, glutamate and ischemia
10) Confidence 0.45 Published 2005 Journal Mol Pain Section Body Doc Link PMC1274343 Disease Relevance 0.39 Pain Relevance 1.08
Does pathological persistent pain cause cellular energy insufficiency that inverses the glutamate transporter operation to release glutamate in the spinal cord?
Localization (release) of glutamate transporter in spinal cord associated with pain, glutamate, lasting pain and spinal cord
11) Confidence 0.42 Published 2005 Journal Mol Pain Section Body Doc Link PMC1274343 Disease Relevance 0.37 Pain Relevance 1.09
On the other hand, the glutamate transporter activator MS-153, which is reported to accelerate glutamate uptake in in vivo and in vitro studies [23-26], had no effect in formalin tests when MS-153 was applied via intrathecal injection, even at the highest dose (1,000 ?
Localization (reported) of glutamate transporter associated with glutamate and intrathecal
12) Confidence 0.39 Published 2005 Journal Mol Pain Section Body Doc Link PMC1274343 Disease Relevance 0.84 Pain Relevance 1.06
In the first four mechanisms, glutamate transporter inhibitors lead to an increase in spinal extracellular glutamate levels, whereas, in the last one, glutamate transporter inhibitors block the reversed glutamate transporter-mediated glutamate release, and reduce extracellular glutamate levels (Fig. 4).
Localization (release) of glutamate transporter-mediated in spinal associated with glutamate
13) Confidence 0.37 Published 2005 Journal Mol Pain Section Body Doc Link PMC1274343 Disease Relevance 0.76 Pain Relevance 1.82
It is possible that blocking the reversed glutamate transporter-mediated glutamate release is an underlying mechanism of antinociception produced by glutamate transporter inhibition under chronic pain conditions.
Localization (release) of glutamate transporter-mediated associated with antinociception, glutamate and lasting pain
14) Confidence 0.37 Published 2005 Journal Mol Pain Section Body Doc Link PMC1274343 Disease Relevance 0.47 Pain Relevance 1.34
This conclusion is consistent with reports on the distribution of GLT-1 and GLAST in hippocampus and cerebellum where the transporters were found to be in astrocytes [18-21].
Localization (distribution) of GLAST in hippocampus associated with hippocampus
15) Confidence 0.20 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.15 Pain Relevance 0.28

General Comments

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