INT6351

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Context Info
Confidence 0.64
First Reported 1982
Last Reported 2010
Negated 0
Speculated 3
Reported most in Body
Documents 40
Total Number 43
Disease Relevance 11.99
Pain Relevance 19.00

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

signal transduction (Gabbr1) plasma membrane (Gabbr1) transcription factor binding (Gabbr1)
cytoplasm (Gabbr1) signal transducer activity (Gabbr1)
Anatomy Link Frequency
neurons 5
brain 4
cerebellar granule cells 1
ileum 1
tail 1
Gabbr1 (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 499 100.00 Very High Very High Very High
Opioid 3 100.00 Very High Very High Very High
antagonist 189 99.96 Very High Very High Very High
adenocard 5 99.92 Very High Very High Very High
Clonidine 3 99.76 Very High Very High Very High
depression 35 99.60 Very High Very High Very High
agonist 709 99.54 Very High Very High Very High
Dopamine 111 99.48 Very High Very High Very High
Calcium channel 17 99.46 Very High Very High Very High
noradrenaline 1 99.38 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 64 99.88 Very High Very High Very High
Depression 36 99.60 Very High Very High Very High
Stress 27 99.04 Very High Very High Very High
Nociception 192 98.88 Very High Very High Very High
Suicidal Behaviour 4 98.62 Very High Very High Very High
Neuropathic Pain 93 98.44 Very High Very High Very High
Anxiety Disorder 195 98.24 Very High Very High Very High
Paranoid Disorders 3 97.30 Very High Very High Very High
INFLAMMATION 51 96.80 Very High Very High Very High
Myeloid Leukemia 9 95.48 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It is then suggested that this effect might depend on an indirect activation of GABAB receptors through release of GABA.
Spec (might) Positive_regulation (activation) of GABAB associated with gaba
1) Confidence 0.64 Published 1992 Journal Neuropharmacology Section Abstract Doc Link 1326728 Disease Relevance 0 Pain Relevance 0.78
conotoxins and Rg1A peptides derived from the venom of marine Conus snails, which are currently in development for the treatment of neuropathic pain, have been shown to inhibit native calcium channel currents by the virtue of activation of GABAB receptors in first order neurons [47].
Positive_regulation (activation) of GABAB in neurons associated with calcium channel and neuropathic pain
2) Confidence 0.50 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.91 Pain Relevance 0.77
Interestingly, a series of experiments with novel ligands at GABAB receptors have also suggested a functional contribution of GABAB(1) expressed in peripheral nociceptive neurons; e.g. ?
Positive_regulation (contribution) of GABAB in neurons associated with nociception
3) Confidence 0.50 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.84 Pain Relevance 0.82
For example, electrophysiological studies have suggested inhibition of neurotransmitter release from presynaptic terminals via baclofen-mediated activation of GABAB receptors [43,45].
Positive_regulation (activation) of GABAB associated with neurotransmitter
4) Confidence 0.47 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.88 Pain Relevance 0.80
How can agonist binding in GABAB1 VFT activate the GABAB2 HD?
Positive_regulation (activate) of GABAB2 associated with agonist
5) Confidence 0.42 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.27
Although no such residues were identified, mutations in TM6 were found to convert the modulator into an agonist, suggesting that the mutated residues are involved in stabilizing the GABAB2 HD into its inactive conformation.
Positive_regulation (stabilizing) of GABAB2 associated with agonist
6) Confidence 0.42 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.22
Indeed, the closure of the GABAB1 VFT has been shown to be responsible for GABAB receptor activation [40], and such a closure activates GABAB2 HD whether it is part of the associated subunit (like in the wild-type heterodimer) or linked to the GABAB1 VFT [23].
Spec (whether) Positive_regulation (activates) of GABAB2
7) Confidence 0.42 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.17
Furthermore, it has been shown that a local increase of GABAB concentrations in higher brain centres results in lasting bilateral analgesia [56].
Positive_regulation (increase) of GABAB in brain associated with analgesia
8) Confidence 0.41 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.44 Pain Relevance 0.63
It is concluded that both GABAA and GABAB receptor activation reduced Straub tail induced by morphine.
Positive_regulation (activation) of GABAB receptor in tail associated with morphine
9) Confidence 0.35 Published 2006 Journal Int. J. Neurosci. Section Abstract Doc Link 16861161 Disease Relevance 0 Pain Relevance 0.75
Aryl-alkylamine (such as fendiline), amino acids like phenylalanine, leucine and isoleucine as well as dipeptides have also been shown to enhance GABAB receptor activity in brain slices [14, 37, 38].
Positive_regulation (enhance) of GABAB receptor in brain
10) Confidence 0.30 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.16
The generation of knockout mice deleted of either the GABAB1 or the GABAB2 gene confirmed a role of GABAB receptor in anxiety [17], as illustrated in several tests such as the light-dark box, the elevated plus maze or the elevated zero maze [18, 55].
Positive_regulation (deleted) of GABAB2 associated with targeted disruption and anxiety disorder
11) Confidence 0.30 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0.89 Pain Relevance 0.16
Indeed, the closure of the GABAB1 VFT has been shown to be responsible for GABAB receptor activation [40], and such a closure activates GABAB2 HD whether it is part of the associated subunit (like in the wild-type heterodimer) or linked to the GABAB1 VFT [23].
Positive_regulation (activation) of GABAB receptor
12) Confidence 0.30 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.17
When examined in brain slices, these compounds potentiated GABAB receptor action on synaptic transmission.
Positive_regulation (potentiated) of GABAB receptor in brain
13) Confidence 0.30 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0.07 Pain Relevance 0.37
Stimulation of GABAB receptors hyperpolarized these cells by activating an inwardly rectifying potassium conductance.
Positive_regulation (Stimulation) of GABAB
14) Confidence 0.29 Published 1996 Journal Neuroendocrinology Section Abstract Doc Link 8857605 Disease Relevance 0 Pain Relevance 0.32
More recent studies indicate that SCS releases substance P serotonin, noradrenaline and GABA in the dorsal horns; activation of the GABAB receptor may be linked to a decrease in the release of glutamate and other excitatory amino acids, resulting in a decrease of neuropathic pain.
Positive_regulation (activation) of GABAB in dorsal horns associated with neuropathic pain, gaba, glutamate, noradrenaline, serotonin, spinal-cord stimulation, substance p and excitatory amino acid
15) Confidence 0.28 Published 2009 Journal Masui Section Abstract Doc Link 19928506 Disease Relevance 1.06 Pain Relevance 1.31
Indeed, activation of GABAB receptors exerts analgesic/antinociceptive effects in animal models of chronic inflammation and neuropathy (see [5]), suppresses drug seeking behavior [15], and has some anxiolytic activity both in animal models and in human [17].
Positive_regulation (activation) of GABAB associated with inflammation, analgesic, anxiety disorder, neuropathic pain and antinociceptive
16) Confidence 0.28 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0.70 Pain Relevance 0.73
In summary, GABAB receptor activation is due to the closure of the GABAB1 VFT, that likely results in a relative movement of one subunit compare to the other.
Positive_regulation (activation) of GABAB receptor
17) Confidence 0.28 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.16
As such, these molecules appear as a better alternative to GABAB agonists, allowing the specific enhancement of GABAB receptor activity when and where needed, and as such, are less prone to tolerance in contrast to the pure agonists that constantly activate the receptor in any region where it is expressed.
Positive_regulation (enhancement) of GABAB receptor associated with tolerance and agonist
18) Confidence 0.28 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0.13 Pain Relevance 0.52
Although drugs activating the GABAB receptor were found to have a number of possible therapeutic actions, these were limited because of tolerance and undesired side effects which include sedation, myorelaxing activity and hypothermia.
Positive_regulation (activating) of GABAB receptor associated with hypothermia, tolerance and sleep disorders
19) Confidence 0.28 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0.58 Pain Relevance 0.59
Indeed, CGP7930 was found to activate GABAB2 subunit expressed alone, as well as a truncated version of this subunit corresponding to the HD only.
Positive_regulation (activate) of GABAB2
20) Confidence 0.28 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.24

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