INT135674

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Context Info
Confidence 0.62
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 15
Disease Relevance 5.21
Pain Relevance 13.61

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
neuronal 6
spinal 2
glial cells 2
Muller cells 2
spinal cord 2
Slc1a3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate 304 100.00 Very High Very High Very High
spinal dorsal horn 15 100.00 Very High Very High Very High
Morphine 70 99.98 Very High Very High Very High
tolerance 8 99.90 Very High Very High Very High
Calcitonin gene-related peptide 109 99.84 Very High Very High Very High
Endep 51 99.70 Very High Very High Very High
Spinal cord 105 99.56 Very High Very High Very High
Antinociceptive 18 99.52 Very High Very High Very High
intrathecal 21 99.00 Very High Very High Very High
cytokine 33 98.42 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nervous System Injury 32 99.98 Very High Very High Very High
Stress 105 99.62 Very High Very High Very High
Pain 115 98.28 Very High Very High Very High
INFLAMMATION 141 98.24 Very High Very High Very High
Nociception 99 97.80 Very High Very High Very High
Glaucoma 56 97.32 Very High Very High Very High
Neuropathic Pain 49 96.92 Very High Very High Very High
Ganglion Cysts 41 91.04 High High
Temporomandibular Joint Syndrome 65 89.68 High High
Anxiety Disorder 20 82.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Co-administration of amitriptyline with morphine attenuated morphine tolerance and up-regulated GLAST and GLT-1 expression.
Positive_regulation (up-regulated) of Gene_expression (expression) of GLAST associated with tolerance, endep and morphine
1) Confidence 0.62 Published 2006 Journal Pain Section Abstract Doc Link 16697108 Disease Relevance 0 Pain Relevance 1.87
The mechanisms involved may include: (a) inhibition of pro-inflammatory cytokine expression, (b) prevention of glutamate transporter down-regulation, and even up-regulation of glial GTs GLAST and GLT-1 expression, with (c) attenuation of morphine-evoked EAA release following continuous long-term morphine infusion.
Positive_regulation (up-regulation) of Gene_expression (expression) of GLAST associated with glutamate, inflammation, morphine and cytokine
2) Confidence 0.45 Published 2006 Journal Pain Section Abstract Doc Link 16697108 Disease Relevance 0.10 Pain Relevance 1.76
Chronic constriction nerve injury upregulated glutamate transporter expression at day 1 and 4 postoperatively, but it downregulated glutamate transporter expression at days 7 and 14 postoperatively [21].
Positive_regulation (upregulated) of Gene_expression (expression) of glutamate transporter in nerve associated with glutamate and nervous system injury
3) Confidence 0.42 Published 2005 Journal Mol Pain Section Body Doc Link PMC1274343 Disease Relevance 0.65 Pain Relevance 1.14
In conclusion, amitriptyline/morphine co-infusion restores the antinociceptive effect of morphine and upregulates GLAST and GLT-1 expression and restores EAAC1 expression to baseline levels, thus reducing excitatory amino acid levels in the spinal CSF dialysates.
Positive_regulation (upregulates) of Gene_expression (expression) of GLAST in CSF associated with antinociceptive, endep, excitatory amino acid and morphine
4) Confidence 0.41 Published 2008 Journal Neuroscience Section Abstract Doc Link 18400403 Disease Relevance 0 Pain Relevance 1.44
We previously showed that intrathecal co-administration of amitriptyline with morphine upregulates the expression of the glial glutamate transporters glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) and restores neuronal glutamate transporter excitatory amino acid carrier 1 (EAAC1) expression in chronically morphine-infused rats.
Positive_regulation (upregulates) of Gene_expression (expression) of glutamate transporter-1 in neuronal associated with glutamate, endep, excitatory amino acid, morphine and intrathecal
5) Confidence 0.41 Published 2008 Journal Neuroscience Section Abstract Doc Link 18400403 Disease Relevance 0 Pain Relevance 0.98
We previously showed that intrathecal co-administration of amitriptyline with morphine upregulates the expression of the glial glutamate transporters glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) and restores neuronal glutamate transporter excitatory amino acid carrier 1 (EAAC1) expression in chronically morphine-infused rats.
Positive_regulation (upregulates) of Gene_expression (expression) of GLAST in neuronal associated with glutamate, endep, excitatory amino acid, morphine and intrathecal
6) Confidence 0.41 Published 2008 Journal Neuroscience Section Abstract Doc Link 18400403 Disease Relevance 0 Pain Relevance 0.97
This suggests that the expression of GLT-1 and GLAST under normal conditions in the spinal dorsal horn primarily originates in astrocytes.
Positive_regulation (originates) of Gene_expression (expression) of GLAST in spinal associated with spinal dorsal horn
7) Confidence 0.35 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.14 Pain Relevance 0.26
However, instead of a reduction, an increased expression of GLAST in the retinal Muller cells was reported using a similar model (Woldemussie et al., 2004), where the authors suggested a compensatory mechanism.
Positive_regulation (increased) of Gene_expression (expression) of GLAST in Muller cells
8) Confidence 0.19 Published 2008 Journal Progress in Brain Research Section Body Doc Link PMC2603274 Disease Relevance 0.58 Pain Relevance 0.41
To our knowledge, this is the first example of using natural products as dietary supplements to increase GLAST expression.
Positive_regulation (increase) of Gene_expression (expression) of GLAST
9) Confidence 0.17 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.27 Pain Relevance 0.65
While GLAST staining was present in glia within the TNC in control animals, GLAST expression was greatly increased in glial cells throughout the TNC in animals treated with GSE (Figure 5A).
Positive_regulation (increased) of Gene_expression (expression) of GLAST in glial cells
10) Confidence 0.17 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.05 Pain Relevance 0.25
Taken together, our findings provide evidence that GSE functions to regulate levels of proteins known to play important roles in regulating spinal neuronal and glial excitability by decreasing CGRP expression and increasing GLAST expression.
Positive_regulation (increasing) of Gene_expression (expression) of GLAST in neuronal associated with calcitonin gene-related peptide
11) Confidence 0.15 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.39 Pain Relevance 0.64
Significantly, we also found that GSE caused increased expression of the glutamate transporter GLAST that functions to regulate the amount of extracellular glutamate.
Positive_regulation (increased) of Gene_expression (expression) of GLAST associated with glutamate
12) Confidence 0.15 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.55 Pain Relevance 0.88
Another interesting finding from our study was that dietary GSE decreases basal expression of the MAP kinase-responsive gene CGRP, while increasing expression of GLAST in the TNC.
Positive_regulation (increasing) of Gene_expression (expression) of GLAST associated with calcitonin gene-related peptide
13) Confidence 0.13 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.98 Pain Relevance 0.91
Gene transfer of GLT-1, a glial glutamate transporter, into the spinal cord by recombinant adenovirus attenuates inflammatory and neuropathic pain in rats

Background

Positive_regulation (transfer) of Gene_expression (transfer) of glutamate transporter in spinal cord associated with glutamate, inflammation, neuropathic pain and spinal cord
14) Confidence 0.08 Published 2008 Journal Mol Pain Section Title Doc Link PMC2628654 Disease Relevance 0.75 Pain Relevance 0.92
Chronic stress has been shown to increase expression of the glutamate transporter, GLT-1, which is important for removing excess glutamate from synaptic regions [158].
Positive_regulation (increase) of Gene_expression (expression) of glutamate transporter associated with stress and glutamate
15) Confidence 0.06 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2701287 Disease Relevance 0.76 Pain Relevance 0.54

General Comments

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