INT74827

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.70
First Reported 1998
Last Reported 2010
Negated 1
Speculated 5
Reported most in Body
Documents 52
Total Number 57
Disease Relevance 26.54
Pain Relevance 50.63

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 cord 26
spinal 14
neuronal 6
striatum 5
hippocampus 4
Slc1a2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate 1280 100.00 Very High Very High Very High
Spinal cord 850 100.00 Very High Very High Very High
Morphine 163 100.00 Very High Very High Very High
spinal dorsal horn 104 100.00 Very High Very High Very High
Thalamus 3 100.00 Very High Very High Very High
withdrawal 191 99.98 Very High Very High Very High
narcan 28 99.90 Very High Very High Very High
tolerance 12 99.90 Very High Very High Very High
Nucleus accumbens 29 99.86 Very High Very High Very High
Inflammation 538 99.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neuropathic Pain 860 99.84 Very High Very High Very High
INFLAMMATION 539 99.84 Very High Very High Very High
Stress 316 99.62 Very High Very High Very High
Nociception 424 99.60 Very High Very High Very High
Hyperalgesia 348 99.32 Very High Very High Very High
Pain 515 98.70 Very High Very High Very High
Nervous System Injury 256 98.32 Very High Very High Very High
Morphine Dependence 15 98.04 Very High Very High Very High
Drug Dependence 23 97.16 Very High Very High Very High
Infection 44 96.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The expression of GLT-1 mRNA was significantly decreased in the striatum and thalamus of morphine-dependent rats, and significantly increased in the striatum 2 h after the naloxone-precipitated withdrawal, compared with that of naive rats.
Positive_regulation (increased) of Gene_expression (expression) of GLT-1 mRNA in thalamus associated with narcan, thalamus, withdrawal and morphine
1) Confidence 0.70 Published 2001 Journal Brain Res. Section Abstract Doc Link 11423104 Disease Relevance 0.17 Pain Relevance 0.99
Formalin injection into one hindpaw caused a rapid transient upregulation of GLT-1 protein expression in the spinal cord which did not occur when rats were pretreated with morphine (10 mg/kg, i.p.) suggesting that the nociceptive input specifically caused the increase of GLT-1 transcription.
Positive_regulation (upregulation) of Gene_expression (expression) of GLT-1 protein in spinal cord associated with nociception, morphine and spinal cord
2) Confidence 0.70 Published 2003 Journal Neuroscience Section Abstract Doc Link 12535941 Disease Relevance 0.57 Pain Relevance 0.32
Effect of gene transfer of GLT-1, a glutamate transporter, into the locus coeruleus by recombinant adenoviruses on morphine physical dependence in rats.
Positive_regulation (transfer) of Gene_expression (transfer) of GLT-1 in locus coeruleus associated with glutamate, physical dependence, locus ceruleus and morphine
3) Confidence 0.69 Published 2004 Journal Eur. J. Neurosci. Section Title Doc Link 14750980 Disease Relevance 0.42 Pain Relevance 1.40
Local overexpression of GLT-1 within the bilateral LC by the recombinant adenoviruses before implantation of the morphine pellet significantly inhibited various somatic signs of naloxone-precipitated morphine withdrawal, compared with the control.
Positive_regulation (overexpression) of Gene_expression (overexpression) of GLT-1 associated with locus ceruleus, narcan, withdrawal and morphine
4) Confidence 0.69 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 14750980 Disease Relevance 0.41 Pain Relevance 1.55
Effect of spinal gene transfer of GLT-1 on neuropathic pain
Positive_regulation (transfer) of Gene_expression (transfer) of GLT-1 in spinal associated with neuropathic pain
5) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 0.89 Pain Relevance 0.70
In contrast to the ability of exogenous GLT-1 to prevent the induction of pathological pain, when the spinal infusion of the adenoviruses was performed 7 or 14 days after pSNL, spinal gene transfer of GLT-1 did not reverse the established allodynia.
Positive_regulation (transfer) of Gene_expression (transfer) of GLT-1 in spinal associated with pain and allodynia
6) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 0.66 Pain Relevance 1.04
These results suggest that adenovirus-mediated overexpression of GLT-1 in the spinal cord prevents the induction of inflammatory and neuropathic pain.
Positive_regulation (overexpression) of Gene_expression (overexpression) of GLT-1 in spinal cord associated with inflammation, neuropathic pain and spinal cord
7) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 1.16 Pain Relevance 1.17
Effect of spinal gene transfer of GLT-1 on inflammatory hyperalgesia
Positive_regulation (transfer) of Gene_expression (transfer) of GLT-1 in spinal associated with hyperalgesia and inflammation
8) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 0.89 Pain Relevance 0.38
Our results suggest that the increase of glutamate uptake activity following overexpression of spinal GLT-1 protein decreases the excessive extracellular glutamate level; this in turn inhibits the generation of neuronal plasticity related to central sensitization following peripheral inflammation and nerve injury.
Positive_regulation (overexpression) of Gene_expression (overexpression) of GLT-1 protein in neuronal associated with glutamate, nervous system injury, inflammation and central sensitization
9) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 1.36 Pain Relevance 1.43
The present study showed that contralateral allodynia was also prevented by the unilateral gene transfer of GLT-1 into the ipsilateral spinal cord, although the unilateral gene transfer did not spread to the contralateral spinal cord.
Positive_regulation (transfer) of Gene_expression (transfer) of GLT-1 in spinal cord associated with allodynia and spinal cord
10) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 1.17 Pain Relevance 1.41
We previously reported that an infusion of Ad-GLT-1 into specific brain areas efficiently increased GLT-1 expression at 2 and 5 days, and this expression remained stable up to 8 days after the infusion [29,30].
Positive_regulation (increased) of Gene_expression (expression) of GLT-1 in brain
11) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 0.39 Pain Relevance 0.29
Using the recombinant adenoviruses, we showed that gene transfer of GLT-1 into the spinal cord had no effect on the acute nociceptive responses to mechanical and thermal stimuli in naive rats.
Positive_regulation (transfer) of Gene_expression (transfer) of GLT-1 in spinal cord associated with nociception and spinal cord
12) Confidence 0.67 Published 2008 Journal Mol Pain Section Body Doc Link PMC2628654 Disease Relevance 0.65 Pain Relevance 0.46
Bilateral infusion of the recombinant adenoviruses into the NAc shell efficiently increased GLT-1 expression surrounding the infusion site, at least during the period 2-8 days after the infusion.
Positive_regulation (increased) of Gene_expression (expression) of GLT-1 in shell associated with nucleus accumbens
13) Confidence 0.67 Published 2005 Journal Eur. J. Neurosci. Section Abstract Doc Link 16324108 Disease Relevance 0 Pain Relevance 1.07
Intra-NAc shell overexpression of GLT-1 before the conditioning significantly attenuated the conditioned place preference induced by methamphetamine or morphine, when compared with control.
Positive_regulation (overexpression) of Gene_expression (overexpression) of GLT-1 in NAc associated with nucleus accumbens and morphine
14) Confidence 0.67 Published 2005 Journal Eur. J. Neurosci. Section Abstract Doc Link 16324108 Disease Relevance 0 Pain Relevance 1.27
Conversely, gene transfer of GLT-1 into spinal cord attenuates inflammatory and neuropathic pain in rats [25]
Positive_regulation (transfer) of Gene_expression (transfer) of GLT-1 in spinal cord associated with inflammation, neuropathic pain and spinal cord
15) Confidence 0.66 Published 2009 Journal Mol Pain Section Body Doc Link PMC2676254 Disease Relevance 0.51 Pain Relevance 0.47
Nigrostriatal denervation does not affect glutamate transporter mRNA expression but subsequent levodopa treatment selectively increases GLT1 mRNA and protein expression in the rat striatum.
Positive_regulation (increases) of Gene_expression (expression) of GLT1 in striatum associated with glutamate and enkephalin
16) Confidence 0.63 Published 2001 Journal J. Neurochem. Section Title Doc Link 11723182 Disease Relevance 0.09 Pain Relevance 0.41
These animals also showed increased GLT1 protein expression, as assessed by immunostaining and western blotting.
Positive_regulation (increased) of Gene_expression (expression) of GLT1
17) Confidence 0.63 Published 2001 Journal J. Neurochem. Section Abstract Doc Link 11723182 Disease Relevance 0.07 Pain Relevance 0.31
We further suggest that levodopa-induced GLT1 overexpression may represent a compensatory mechanism preventing neurotoxic accumulation of endogenous glutamate.
Positive_regulation (overexpression) of Gene_expression (overexpression) of GLT1 associated with glutamate
18) Confidence 0.63 Published 2001 Journal J. Neurochem. Section Abstract Doc Link 11723182 Disease Relevance 0.05 Pain Relevance 0.31
Using astroglial cultures prepared from the rat cerebral cortex, we found that the delta-opioid receptor agonist [D-pen2,D-pen5]-enkephalin decreases and glutamate increases the expression of the GLT-1 transporter mRNA.
Positive_regulation (increases) of Gene_expression (expression) of GLT-1 transporter mRNA in cerebral cortex associated with glutamate, agonist, enkephalin, opioid receptor and cerebral cortex
19) Confidence 0.62 Published 1998 Journal FEBS Lett. Section Abstract Doc Link 9563512 Disease Relevance 0 Pain Relevance 0.67
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 GLT-1 associated with glutamate, inflammation, morphine and cytokine
20) Confidence 0.58 Published 2006 Journal Pain Section Abstract Doc Link 16697108 Disease Relevance 0.10 Pain Relevance 1.76

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox