INT3440

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Context Info
Confidence 0.57
First Reported 1978
Last Reported 2010
Negated 4
Speculated 4
Reported most in Abstract
Documents 221
Total Number 225
Disease Relevance 33.94
Pain Relevance 180.36

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

mitochondrion (Abat)
Anatomy Link Frequency
neurons 43
nerve 16
cerebral cortex 10
substantia nigra 8
inferior colliculus 8
Abat (Rattus norvegicus)
Pain Link Frequency Relevance Heat
gABA 2382 100.00 Very High Very High Very High
Dopamine 1658 100.00 Very High Very High Very High
Glutamate 894 100.00 Very High Very High Very High
GABAergic 666 100.00 Very High Very High Very High
antagonist 580 100.00 Very High Very High Very High
Neurotransmitter 239 100.00 Very High Very High Very High
tetrodotoxin 213 100.00 Very High Very High Very High
Action potential 195 100.00 Very High Very High Very High
Serotonin 167 100.00 Very High Very High Very High
substance P 92 100.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neuropathic Pain 20 100.00 Very High Very High Very High
Hypoxia 62 99.98 Very High Very High Very High
Injury 52 99.72 Very High Very High Very High
Urological Neuroanatomy 297 99.68 Very High Very High Very High
Pressure Volume 2 Under Development 5 99.62 Very High Very High Very High
INFLAMMATION 66 99.60 Very High Very High Very High
Convulsion 71 99.56 Very High Very High Very High
Pressure And Volume Under Development 9 99.52 Very High Very High Very High
Nervous System Injury 11 99.40 Very High Very High Very High
Pain 140 99.26 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, the efficacies of TTX for inhibition of 4AP-evoked glutamate release were greater than for inhibition of GABA release in all regions except spinal cord.
Negative_regulation (inhibition) of Localization (release) of GABA in spinal cord associated with tetrodotoxin, gaba, glutamate and spinal cord
1) Confidence 0.57 Published 2010 Journal J. Neurochem. Section Abstract Doc Link 20374421 Disease Relevance 0 Pain Relevance 1.09
Potencies of TTX for inhibition of glutamate and GABA release varied between CNS regions.
Negative_regulation (inhibition) of Localization (release) of GABA associated with tetrodotoxin, gaba and glutamate
2) Confidence 0.50 Published 2010 Journal J. Neurochem. Section Abstract Doc Link 20374421 Disease Relevance 0 Pain Relevance 1.10
GABA immunohistochemistry revealed lower GABA content in processes and neuronal somata suggesting diminished GABA release onto pyramidal neurons.
Negative_regulation (diminished) of Localization (release) of GABA in pyramidal neurons associated with gaba and pyramidal cell
3) Confidence 0.46 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18706433 Disease Relevance 0 Pain Relevance 0.70
The most parsimonious explanation for the inhibition of GABA release by a CB receptor inverse agonist is via the disinhibition of an cannabinoid-sensitive inhibitory input onto GABAergic neurones.
Negative_regulation (inhibition) of Localization (release) of GABA associated with gaba, gabaergic, cannabinoid and agonist
4) Confidence 0.45 Published 2010 Journal J. Neuroendocrinol. Section Abstract Doc Link 20236227 Disease Relevance 0.13 Pain Relevance 1.71
In the absence of TTX, however, the opposite effects were observed: WIN 55,212-2 had no effect while rimonabant inhibited GABA release.
Negative_regulation (inhibited) of Localization (release) of GABA associated with tetrodotoxin and gaba
5) Confidence 0.45 Published 2010 Journal J. Neuroendocrinol. Section Abstract Doc Link 20236227 Disease Relevance 0.14 Pain Relevance 1.54
The inhibitory effect of rimonabant was also prevented by naloxone and a kappa-opioid receptor selective antagonist, suggesting that GABA release from arcuate NPY/AgRP/GABA neurones can be inhibited by endogenous opioid peptides, and that the release of opioid peptides is sensitive to cannabinoids.
Negative_regulation (inhibited) of Localization (release) of GABA associated with gaba, cannabinoid, antagonist, endogenous opioid, kappa opioid receptor, narcan and opioid
6) Confidence 0.45 Published 2010 Journal J. Neuroendocrinol. Section Abstract Doc Link 20236227 Disease Relevance 0 Pain Relevance 1.54
In our in vitro model, K(+)-evoked GABA release was inhibited by the endogenous opioid peptide beta-endorphin in a naloxone-sensitive manner.
Negative_regulation (inhibited) of Localization (release) of GABA associated with gaba, narcan and endogenous opioid
7) Confidence 0.45 Published 2010 Journal J. Neuroendocrinol. Section Abstract Doc Link 20236227 Disease Relevance 0.11 Pain Relevance 1.68
L-Aspartic acid only reduced the GABA release, whereas kainic acid exhibited only a marked enhancement of its release.
Negative_regulation (reduced) of Localization (release) of GABA associated with gaba
8) Confidence 0.43 Published 1981 Journal Brain Res. Section Abstract Doc Link 6118201 Disease Relevance 0 Pain Relevance 0.41
Altogether, these results suggest that reduction of the depolarization-evoked GABA release might contribute to thiopental anesthesia, but this seems unlikely for volatile anesthetics.
Negative_regulation (reduction) of Localization (release) of GABA associated with anesthesia and gaba
9) Confidence 0.43 Published 1995 Journal Brain Res. Section Abstract Doc Link 7743195 Disease Relevance 0 Pain Relevance 0.68
Hypothalamic superfusion with the neutrotoxin tetrodotoxin (1 mumol/l) led to a long-lasting decrease in the GABA release.
Negative_regulation (decrease) of Localization (release) of GABA associated with tetrodotoxin and gaba
10) Confidence 0.43 Published 1993 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 8510767 Disease Relevance 0.39 Pain Relevance 0.65
We conclude that NO may be directly acting on GABA nerve terminals and tonically inhibiting GABA release or synthesis under basal conditions.
Negative_regulation (inhibiting) of Localization (release) of GABA in nerve associated with gaba
11) Confidence 0.43 Published 1995 Journal Neuroreport Section Abstract Doc Link 7488740 Disease Relevance 0 Pain Relevance 0.45
In the absence of Ca2+, the K+-induced release of aspartate, glutamate, and GABA was blocked whereas the K+-induced release of taurine was still present.
Negative_regulation (blocked) of Localization (release) of GABA associated with gaba and glutamate
12) Confidence 0.43 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2872275 Disease Relevance 0 Pain Relevance 0.45
[D-Pro4,D-Trp7,9,10]substance P4-11 (10-15 microM) inhibited the GABA release evoked by substance P, somatostatin and compound 48/80.
Negative_regulation (inhibited) of Localization (release) of GABA associated with gaba, somatostatin and substance p
13) Confidence 0.43 Published 1991 Journal Neuroscience Section Abstract Doc Link 1722288 Disease Relevance 0 Pain Relevance 1.15
The results are compatible with the presence in the rat cerebral cortex of autoreceptors mediating inhibition of GABA release and belonging to the GABAB type.
Negative_regulation (inhibition) of Localization (release) of GABA in cerebral cortex associated with gaba and cerebral cortex
14) Confidence 0.41 Published 1989 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2547942 Disease Relevance 0 Pain Relevance 0.72
The results support the hypothesis that 5-HT(1B) receptors within the VTA can function as heteroreceptors to inhibit GABA release.
Negative_regulation (inhibit) of Localization (release) of GABA associated with ventral tegmentum and gaba
15) Confidence 0.41 Published 2001 Journal J. Neurochem. Section Abstract Doc Link 11723184 Disease Relevance 0 Pain Relevance 0.89
An antiakinetic dose of UFP-512 (10 microg/kg) decreased GABA in globus pallidus (GP) as well as GABA and glutamate (GLU) release in substantia nigra reticulata (SNr).
Negative_regulation (decreased) of Localization (release) of GABA in substantia nigra associated with glutamate, gaba and substantia nigra
16) Confidence 0.41 Published 2009 Journal Neuroscience Section Abstract Doc Link 19729051 Disease Relevance 0.17 Pain Relevance 0.75
These findings are consistent with the proposed mechanism of action of morphine in the lateral ventrocaudal PAG and offer the first direct evidence that systemic opiates decrease GABA release in this midbrain region.
Negative_regulation (decrease) of Localization (release) of GABA in midbrain associated with gaba, midbrain, opiate, central grey and morphine
17) Confidence 0.40 Published 1992 Journal Brain Res. Section Abstract Doc Link 1450948 Disease Relevance 0.54 Pain Relevance 1.13
The response to EDA was partially inhibited by 3-mercaptopropionic acid, a known inhibitor of GABA release.
Negative_regulation (inhibitor) of Localization (release) of GABA associated with gaba
18) Confidence 0.40 Published 1989 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 2555721 Disease Relevance 0 Pain Relevance 0.60
Resolution of the question of whether enkephalins elicit epileptogenic activity and autonomic dysfunction via inhibition of GABA release is important since an understanding of this mechanism should eventually allow the design of pharmacologic agents to prevent the epileptogenic activity, autonomic dysfunction and the associated sudden death.
Negative_regulation (inhibition) of Localization (release) of GABA in autonomic associated with gaba, enkephalin and sudden death
19) Confidence 0.40 Published 1987 Journal Med. Hypotheses Section Abstract Doc Link 3614001 Disease Relevance 0.66 Pain Relevance 0.73
The present study indicates that activation of presynaptic mu-opioid receptors coupled to G-proteins inhibits GABA release through unknown intracellular mechanisms downstream of Ca(2+) influx.
Negative_regulation (inhibits) of Localization (release) of GABA associated with gaba and mu opioid receptor
20) Confidence 0.39 Published 2004 Journal Neurosci. Res. Section Abstract Doc Link 15488297 Disease Relevance 0.25 Pain Relevance 0.72

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