INT99539

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.67
First Reported 2001
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 25
Total Number 25
Disease Relevance 5.46
Pain Relevance 23.38

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 (Slc1a2)
Anatomy Link Frequency
spinal 3
astrocyte 3
cortex 2
brain 1
striatum 1
Slc1a2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate 380 100.00 Very High Very High Very High
tolerance 46 100.00 Very High Very High Very High
Antinociceptive 24 100.00 Very High Very High Very High
Endep 49 99.98 Very High Very High Very High
withdrawal 30 99.98 Very High Very High Very High
Neuropathic pain 53 99.84 Very High Very High Very High
antinociception 6 99.82 Very High Very High Very High
Morphine 156 99.80 Very High Very High Very High
Pain 48 99.72 Very High Very High Very High
excitatory amino acid 31 99.56 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neuropathic Pain 86 99.84 Very High Very High Very High
Stress 105 99.82 Very High Very High Very High
Schizophrenia 10 99.40 Very High Very High Very High
Low Back Pain 2 99.08 Very High Very High Very High
INFLAMMATION 47 98.24 Very High Very High Very High
Injury 10 97.96 Very High Very High Very High
Pain 46 97.52 Very High Very High Very High
Psychosis 8 97.36 Very High Very High Very High
Nervous System Injury 47 96.48 Very High Very High Very High
Hyperalgesia 24 96.08 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results suggest that maintaining a low extracellular glutamate level following an increase in spinal GLT-1 protein does not affect acute spinal pain transmission under normal conditions.
Positive_regulation (increase) of GLT-1 protein in spinal associated with low back pain, pain and glutamate
1) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 0.90 Pain Relevance 0.71
The results from the above suggest that the decrease in GLT-1 and GLAST, which was induced by PNSL, mainly occurred in astrocytes on the injured side.


Positive_regulation (induced) of GLT-1 in astrocytes
2) Confidence 0.66 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.23 Pain Relevance 0.08
Upregulation of GLT-1 and GLAST in microglia following PSNL
Positive_regulation (Upregulation) of GLT-1 in microglia
3) Confidence 0.66 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.31 Pain Relevance 0.07
optic nerve, there appears to be an acute increase in GLT1
Positive_regulation (increase) of GLT1 in optic nerve
4) Confidence 0.53 Published 2007 Journal Experimental Diabetes Research Section Body Doc Link PMC1940058 Disease Relevance 0.68 Pain Relevance 0.41
Amitriptyline upregulates EAAT1 and EAAT2 in neuropathic pain rats.
Positive_regulation (upregulates) of EAAT2 associated with neuropathic pain and endep
5) Confidence 0.51 Published 2010 Journal Brain Res. Bull. Section Title Doc Link 19772901 Disease Relevance 0.36 Pain Relevance 1.08
They activate the glutamate transporter subtype 1 (GLT-1), the protein responsible for 90% of glutamate uptake in the mammalian brain.
Positive_regulation (activate) of GLT-1 in brain associated with glutamate
6) Confidence 0.47 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18644397 Disease Relevance 0.06 Pain Relevance 0.57
Beta-lactam antibiotic reduces morphine analgesic tolerance in rats through GLT-1 transporter activation.
Positive_regulation (activation) of GLT-1 associated with analgesic, tolerance and morphine
7) Confidence 0.47 Published 2010 Journal Drug Alcohol Depend Section Title Doc Link 20004063 Disease Relevance 0 Pain Relevance 1.31
Identification of beta-lactam antibiotics as pharmaceuticals which activate GLT-1 transporters prompted us to hypothesize that repeated beta-lactam antibiotic (ceftriaxone) administration blocks development of tolerance to morphine antinociception through GLT-1 activation.
Positive_regulation (activation) of GLT-1 associated with antinociception, tolerance and morphine
8) Confidence 0.47 Published 2010 Journal Drug Alcohol Depend Section Abstract Doc Link 20004063 Disease Relevance 0 Pain Relevance 1.18
Identification of beta-lactam antibiotics as pharmaceuticals which activate GLT-1 transporters prompted us to hypothesize that repeated beta-lactam antibiotic (ceftriaxone) administration blocks development of tolerance to morphine antinociception through GLT-1 activation.
Positive_regulation (activate) of GLT-1 associated with antinociception, tolerance and morphine
9) Confidence 0.47 Published 2010 Journal Drug Alcohol Depend Section Abstract Doc Link 20004063 Disease Relevance 0 Pain Relevance 0.96
Upregulation or functional enhancement of spinal GLT-1 could be a novel strategy for the prevention of pathological pain.



Positive_regulation (Upregulation) of GLT-1 in spinal associated with pain
10) Confidence 0.45 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2628654 Disease Relevance 0.91 Pain Relevance 0.98
Daily intrathecal injection of Ro106-9920 prevented the amitriptyline/morphine-induced NF-kappaB p65 translocation and reversed the amitriptyline/morphine-induced GLAST and GLT-1 upregulation and inhibited the restoration of EAAC1 expression.
Positive_regulation (upregulation) of GLT-1 associated with endep, morphine and intrathecal
11) Confidence 0.44 Published 2008 Journal Neuroscience Section Abstract Doc Link 18400403 Disease Relevance 0 Pain Relevance 1.68
MDMA induced enhancements in the EAAT 2-2 mRNA level in the forebrain cortex may therefore partly contribute to psychotic effects of this drug.
Positive_regulation (enhancements) of EAAT 2-2 mRNA in cortex associated with psychosis
12) Confidence 0.43 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2358913 Disease Relevance 0.72 Pain Relevance 0.53
In contrast, animals with the lesion subsequently treated with levodopa showed a selective increase (36%) in GLT1 mRNA levels in the denervated striatum versus controls.
Positive_regulation (increase) of GLT1 in striatum
13) Confidence 0.42 Published 2001 Journal J. Neurochem. Section Abstract Doc Link 11723182 Disease Relevance 0.07 Pain Relevance 0.30
These results suggest that GLT1 in hippocampal neurons can be induced to translocate to the nerve terminals and express on the cell surface during morphine withdrawal.
Positive_regulation (induced) of GLT1 in nerve associated with withdrawal and morphine
14) Confidence 0.38 Published 2003 Journal J. Neurosci. Section Abstract Doc Link 12805317 Disease Relevance 0 Pain Relevance 1.18
Morphine withdrawal increases glutamate uptake and surface expression of glutamate transporter GLT1 at hippocampal synapses.
Positive_regulation (increases) of GLT1 in synapses associated with glutamate, withdrawal and morphine
15) Confidence 0.33 Published 2003 Journal J. Neurosci. Section Title Doc Link 12805317 Disease Relevance 0 Pain Relevance 1.15
Long-term morphine infusion induced antinociceptive tolerance and down-regulation of glutamate transporters (GTs), GLAST, GLT-1, and EAAC1, expression in the rat spinal cord dorsal horn.
Positive_regulation (induced) of GLT-1 in spinal cord dorsal horn associated with glutamate, dorsal horn, tolerance, antinociceptive, spinal cord and morphine
16) Confidence 0.33 Published 2007 Journal Pain Section Abstract Doc Link 17346885 Disease Relevance 0 Pain Relevance 1.62
Regarding glutamate transporters, EAAT1 (GLAST) and EAAT2-2 (Glt1b/EAAT2b) (splice variant of EAAT2/Glt1) were significantly increased at the highest administered MDMA dose in the cortex.
Positive_regulation (increased) of EAAT2 in cortex associated with glutamate
17) Confidence 0.31 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2358913 Disease Relevance 0 Pain Relevance 0.81
Upregulation of GLT-1 was also observed (204+/-20% of basal).
Positive_regulation (Upregulation) of GLT-1
18) Confidence 0.31 Published 2005 Journal Neuroscience Section Abstract Doc Link 15893883 Disease Relevance 0 Pain Relevance 1.76
These results show that acute amitriptyline treatment preserved morphine's antinociceptive effect in morphine-tolerant rats; the mechanisms may be involved in inhibition of phospho-PKA and PKC expression, and thus inducing the GLAST and GLT-1 trafficking onto glial cell surface which enhances the EAA uptake from the synaptic cleft and reduces EAA concentration in the spinal CSF.
Positive_regulation (inducing) of GLT-1 in synaptic cleft associated with antinociceptive, endep and morphine
19) Confidence 0.29 Published 2007 Journal Pain Section Abstract Doc Link 17346885 Disease Relevance 0 Pain Relevance 1.54
Here we show that the downregulation of spinal GTs (EAAC1 and GLT-1) induced by a 6-day intrathecal morphine (10 microg, twice daily) treatment regimen was prevented by co-administration of morphine with 2',5'-dideoxyadenosine (ddA, 1 microg, a broad adenylyl cyclase inhibitor) or H89 (10 microg, a selective protein kinase A inhibitor).
Positive_regulation (induced) of GLT-1 in spinal associated with morphine and intrathecal
20) Confidence 0.28 Published 2005 Journal Neurosci. Lett. Section Abstract Doc Link 15694265 Disease Relevance 0.06 Pain Relevance 0.74

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox