INT6352

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Context Info
Confidence 0.59
First Reported 1992
Last Reported 2009
Negated 0
Speculated 2
Reported most in Body
Documents 7
Total Number 14
Disease Relevance 4.84
Pain Relevance 7.93

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 3
neuronal 1
spinal 1
postsynaptic membrane 1
brain 1
Gabbr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Analgesic 14 100.00 Very High Very High Very High
Neurotransmitter 57 99.84 Very High Very High Very High
cocaine 25 99.84 Very High Very High Very High
antinociception 24 99.44 Very High Very High Very High
nociceptor 126 98.64 Very High Very High Very High
Dopamine 18 98.36 Very High Very High Very High
midbrain 2 98.18 Very High Very High Very High
Sumatriptan 4 98.08 Very High Very High Very High
opioid receptor 4 96.64 Very High Very High Very High
agonist 100 96.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nociception 288 99.44 Very High Very High Very High
Inflammatory Pain 36 94.28 High High
Pain 188 94.04 High High
Neuropathic Pain 115 85.76 High High
Hyperalgesia 48 85.00 Quite High
Hypersensitivity 30 83.68 Quite High
Congenital Anomalies 12 76.16 Quite High
INFLAMMATION 55 73.60 Quite High
Nervous System Injury 25 69.36 Quite High
Peripheral Neuropathy 6 69.20 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results imply that a loss of GABAB receptors in nociceptive DRG neurons does not produce a major effect on nociceptive behavior and is not involved in the modulation of chronic inflammatory pain.


Negative_regulation (loss) of GABAB in neurons associated with nociception and ipn
1) Confidence 0.59 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 1.31 Pain Relevance 0.83
Therefore, based upon our findings, we infer that a conditional loss of GABAB receptor function in peripheral nociceptive neurons in vivo does not lead to significant changes in nociception and the development of pathological pain.
Negative_regulation (loss) of GABAB in neurons associated with nociception and pain
2) Confidence 0.59 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.74 Pain Relevance 0.48
Numerous studies in cell lines as well as native tissues have demonstrated that a loss of GABAB(1) leads to a complete lack of ligand binding and a total loss of function of native GABAB receptors [28,36-38].
Negative_regulation (loss) of GABAB
3) Confidence 0.51 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.89 Pain Relevance 0.54
These mice are well-suited for elucidating the relevance of GABAB receptor-mediated presynaptic inhibition of neurotransmitter release from nociceptor terminals as well as a putative role for GABAB receptors in peripheral nociceptive terminals in physiological and pathophysiological states.
Negative_regulation (inhibition) of GABAB in nociceptor associated with nociception, neurotransmitter and nociceptor
4) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 1.02 Pain Relevance 1.07
Therefore, the phenotype in phase IIb of the formalin response could be caused by exaggerated activation of primary afferents due to the lack of GABAB mediated inhibition in the first phase of the formalin test.
Negative_regulation (inhibition) of GABAB
5) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.70 Pain Relevance 0.34
SNS-GABAB(1)-/- mice showed a selective deletion of GABAB(1) in small diameter neurons of the DRG whereas expression in large-diameter neurons was preserved (Fig. 1C).


Negative_regulation (deletion) of GABAB in neurons
6) Confidence 0.43 Published 2009 Journal Mol Pain Section Body Doc Link PMC2785766 Disease Relevance 0.12 Pain Relevance 0.38
Here, we identified a
novel secreted GABAB1 isoform containing the SDs and addressed
whether such soluble isoforms have the potential to block neuronal
GABAB receptor functions in a dominant-negative manner.
Spec (whether) Negative_regulation (block) of GABAB in neuronal
7) Confidence 0.43 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2576543 Disease Relevance 0 Pain Relevance 0
In contrast,
soluble SD protein neither impairs the activity of GABAB
autoreceptors nor impairs the activity of postsynaptic GABAB
receptors. 
Negative_regulation (impairs) of GABAB
8) Confidence 0.43 Published 2008 Journal The Journal of Biological Chemistry Section Abstract Doc Link PMC2576543 Disease Relevance 0.06 Pain Relevance 0.14
Desensitization of GABAB receptors and antagonism by CGP 35348, prevent bicuculline- and picrotoxin-induced antinociception.
Negative_regulation (Desensitization) of GABAB associated with antinociception and analgesic
9) Confidence 0.40 Published 1992 Journal Neuropharmacology Section Title Doc Link 1326728 Disease Relevance 0 Pain Relevance 0.68
Eventually, mice lacking either GABAB1 or GABAB2 share very similar phenotypes, and none of the known GABAB-mediated responses could be measured in either mice [66, 69].
Negative_regulation (lacking) of GABAB1
10) Confidence 0.26 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2656813 Disease Relevance 0 Pain Relevance 0.07
The present study was designed to investigate the modulatory effects of blockade of spinal GABAA and GABAB receptors on antinociception induced by supraspinally administered mu- and epsilon-opioid receptor agonists.
Spec (investigate) Negative_regulation (blockade) of GABAB in spinal associated with antinociception, agonist and opioid receptor
11) Confidence 0.10 Published 1996 Journal Eur. J. Pharmacol. Section Abstract Doc Link 8832215 Disease Relevance 0 Pain Relevance 0.88
While DSI and DPI rely on retrograde messengers, rebound potentiation is a purely postsynaptic phenomenon, where the main regulatory players in the postsynaptic membrane seem to be GABAB and mGluRI receptors.
Negative_regulation (receptors) of GABAB in postsynaptic membrane
12) Confidence 0.03 Published 2008 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2526003 Disease Relevance 0 Pain Relevance 0.03
Using intracellular recordings from midbrain dopamine neurons in a brain slice preparation, we have found that cocaine (0.1-10 microM) inhibited the GABAB IPSP in a dose-dependent manner.
Negative_regulation (inhibited) of GABAB IPSP in brain associated with dopamine, midbrain and cocaine
13) Confidence 0.02 Published 1994 Journal J. Neurosci. Section Abstract Doc Link 7965077 Disease Relevance 0 Pain Relevance 1.12
Pretreatment of slices with the 5-HT-depleting agent p-chloroamphetamine (pCA; 10 microM) abolished the inhibition of the GABAB IPSP by cocaine but failed to affect the actions of sumatriptan.
Negative_regulation (inhibition) of GABAB IPSP associated with sumatriptan and cocaine
14) Confidence 0.02 Published 1994 Journal J. Neurosci. Section Abstract Doc Link 7965077 Disease Relevance 0 Pain Relevance 1.35

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