INT16850

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Context Info
Confidence 0.51
First Reported 1983
Last Reported 2011
Negated 2
Speculated 0
Reported most in Abstract
Documents 73
Total Number 73
Disease Relevance 8.28
Pain Relevance 47.89

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

transport (Gabrg1) plasma membrane (Gabrg1)
Anatomy Link Frequency
external 8
interneurons 6
neurons 6
small intestine 4
cerebral cortex 4
Gabrg1 (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 1068 100.00 Very High Very High Very High
Glutamate 136 100.00 Very High Very High Very High
Action potential 130 100.00 Very High Very High Very High
antagonist 129 100.00 Very High Very High Very High
Neurotransmitter 120 100.00 Very High Very High Very High
tetrodotoxin 71 100.00 Very High Very High Very High
Catecholamine 7 100.00 Very High Very High Very High
Hippocampus 98 99.92 Very High Very High Very High
Morphine 233 99.84 Very High Very High Very High
Dopamine 195 99.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pressure And Volume Under Development 5 99.90 Very High Very High Very High
Targeted Disruption 117 98.70 Very High Very High Very High
Urological Neuroanatomy 35 98.16 Very High Very High Very High
Ganglion Cysts 57 97.36 Very High Very High Very High
Death 6 97.20 Very High Very High Very High
Aggression 4 95.20 Very High Very High Very High
Rheumatoid Arthritis 5 95.12 Very High Very High Very High
Catalepsy 17 94.16 High High
Tremor 1 94.16 High High
Nociception 10 93.60 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Veratridine- (sodium channel-) dependent release of the neurotransmitters L-glutamate and GABA was almost fully inhibited by 20(S)-protopanaxadiol, however, less complete inhibition was observed with Rh(2).
Negative_regulation (inhibited) of Localization (release) of GABA associated with gaba, glutamate, neurotransmitter and sodium channel
1) Confidence 0.51 Published 2008 Journal Comp. Biochem. Physiol. C Toxicol. Pharmacol. Section Abstract Doc Link 18262850 Disease Relevance 0 Pain Relevance 0.75
Studies on the ionic dependence showed that the stimulation of GABA release by EGTA was abolished in a Na+-free medium.
Negative_regulation (abolished) of Localization (release) of GABA associated with addiction and gaba
2) Confidence 0.42 Published 1984 Journal J. Neurochem. Section Abstract Doc Link 6144725 Disease Relevance 0 Pain Relevance 0.60
A Na+ channel blocker, tetrodotoxin did not reduce GABA-evoked CA release.
Neg (not) Negative_regulation (reduce) of Localization (release) of GABA associated with tetrodotoxin, gaba and catecholamine
3) Confidence 0.39 Published 1984 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 6472489 Disease Relevance 0 Pain Relevance 1.10
The Ca(2+)-dependent fraction of the [3H]GABA released by high K+ depolarization is also completely abolished by amiloride (from 300 microM) and sensitive to verapamil (30 microM), but in contrast is insensitive to the absence of external Na+ and to DABA.
Negative_regulation (abolished) of Localization (released) of GABA in external associated with gaba
4) Confidence 0.38 Published 1993 Journal Neurochem. Res. Section Abstract Doc Link 8255356 Disease Relevance 0 Pain Relevance 0.52
On the basis of these results we conclude that amiloride and verapamil inhibit high K(+)-induced release of [3H]GABA by antagonizing the entrance of Ca2+ (and possibly Na+ when external Ca2+ is absent) through a population of voltage sensitive presynaptic Ca2+ channels activated by depolarization.
Negative_regulation (inhibit) of Localization (release) of GABA in external associated with gaba
5) Confidence 0.38 Published 1993 Journal Neurochem. Res. Section Abstract Doc Link 8255356 Disease Relevance 0 Pain Relevance 0.47
The absence of external Na+ completely abolishes the release of the carrier-mediated, presumably cytoplasmic release of [3H]GABA induced by homoexchange and heteroexchange with GABA and DABA, respectively.
Negative_regulation (abolishes) of Localization (release) of GABA in external associated with gaba
6) Confidence 0.38 Published 1993 Journal Neurochem. Res. Section Abstract Doc Link 8255356 Disease Relevance 0 Pain Relevance 0.52
The absence of external Na+ completely abolishes the release of the carrier-mediated, presumably cytoplasmic release of [3H]GABA induced by homoexchange and heteroexchange with GABA and DABA, respectively.
Negative_regulation (abolishes) of Localization (release) of GABA in external associated with gaba
7) Confidence 0.38 Published 1993 Journal Neurochem. Res. Section Abstract Doc Link 8255356 Disease Relevance 0 Pain Relevance 0.52
This Na+ dependence does not seem to involve voltage-sensitive channels, since tetrodotoxin did not affect the GABA-releasing action of EGTA, whereas in parallel superfusion chambers it blocked over 80% the stimulation of GABA release by veratridine.
Negative_regulation (blocked) of Localization (release) of GABA associated with tetrodotoxin, addiction and gaba
8) Confidence 0.37 Published 1984 Journal J. Neurochem. Section Abstract Doc Link 6144725 Disease Relevance 0 Pain Relevance 0.70
The electrical transmural stimulation-evoked release of labeled and endogenous GABA was inhibited by superfusion with tetrodotoxin and Ca2+-free Krebs-Ringer solution containing 1 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid.
Negative_regulation (inhibited) of Localization (release) of GABA associated with tetrodotoxin and gaba
9) Confidence 0.37 Published 1983 Journal Am. J. Physiol. Section Abstract Doc Link 6638195 Disease Relevance 0 Pain Relevance 0.65
GABA release by veratrine was blocked by tetrodotoxin.
Negative_regulation (blocked) of Localization (release) of GABA associated with tetrodotoxin and gaba
10) Confidence 0.36 Published 1987 Journal Brain Res. Section Abstract Doc Link 3594247 Disease Relevance 0.19 Pain Relevance 0.34
This NA-induced GABA release was suppressed by tetrodotoxin, a sodium channel blocker, which was perfused at the probe site.
Negative_regulation (suppressed) of Localization (release) of GABA associated with tetrodotoxin, gaba, sodium channel and noradrenaline
11) Confidence 0.36 Published 1994 Journal Neuroreport Section Abstract Doc Link 7865739 Disease Relevance 0 Pain Relevance 0.73
The release of GABA was also induced by veratrine and blocked by tetrodotoxin.
Negative_regulation (blocked) of Localization (release) of GABA associated with tetrodotoxin and gaba
12) Confidence 0.36 Published 1983 Journal Brain Res. Section Abstract Doc Link 6871712 Disease Relevance 0 Pain Relevance 0.37
The GABA-induced acid secretion was inhibited by bicuculline, scopolamine, pirenzepine, proglumide, and tetrodotoxin, but not by cimetidine.
Negative_regulation (inhibited) of Localization (secretion) of GABA associated with tetrodotoxin and gaba
13) Confidence 0.36 Published 1987 Journal Am. J. Physiol. Section Abstract Doc Link 3688228 Disease Relevance 0 Pain Relevance 0.53
Non-opioid analgesia of the neuropeptide, neo-kyotorphin and possible mediation by inhibition of GABA release in the mouse brain.
Negative_regulation (inhibition) of Localization (release) of GABA in brain associated with gaba, analgesic, neuropeptide, opioid and analgesia
14) Confidence 0.35 Published 1987 Journal Peptides Section Title Doc Link 3432136 Disease Relevance 0 Pain Relevance 1.05
Neo-kyotorphin inhibited the Ca2+-dependent and depolarization-evoked release of 3H-GABA, from crude synaptosomes of the lower brain stem of rats.
Negative_regulation (inhibited) of Localization (release) of GABA in brain stem associated with gaba
15) Confidence 0.35 Published 1987 Journal Peptides Section Abstract Doc Link 3432136 Disease Relevance 0 Pain Relevance 0.91
When misoprostol was perfused in combination with the peripheral injection of formalin, we observed an increase of glutamate and an increase followed by a stronger decrease in GABA release.
Negative_regulation (decrease) of Localization (release) of GABA associated with gaba and glutamate
16) Confidence 0.34 Published 2006 Journal Eur. J. Pharmacol. Section Abstract Doc Link 16360148 Disease Relevance 0.93 Pain Relevance 0.91
In addition, TTX blockade of sodium-dependent action potentials itself would have significantly reduced the spike-mediated release of GABA, glycine, glutamate, acetylcholine, and dopamine by amacrine and ganglion cells of the inner retina, reinforcing the negative findings with the pharmacological blockers specific to each of these transmitter systems.
Negative_regulation (reduced) of Localization (release) of GABA in retina associated with ganglion cysts, action potential, tetrodotoxin, dopamine, glutamate and gaba
17) Confidence 0.34 Published 2008 Journal PLoS Biology Section Body Doc Link PMC2567003 Disease Relevance 0.10 Pain Relevance 0.61
Immunolocalization of GABAA receptor subunits was hampered, due to availability of suitable antisera, but localization of GABAA-?
Negative_regulation (hampered) of Localization (localization) of GABAA
18) Confidence 0.34 Published 2004 Journal Reprod Biol Endocrinol Section Body Doc Link PMC416489 Disease Relevance 0 Pain Relevance 0.30
Immunolocalization of GABAA receptor subunits was hampered, due to availability of suitable antisera, but localization of GABAA-?
Negative_regulation (hampered) of Localization (localization) of GABAA
19) Confidence 0.34 Published 2004 Journal Reprod Biol Endocrinol Section Body Doc Link PMC416489 Disease Relevance 0 Pain Relevance 0.30
Diazepam, clonazepam and pentobarbital potentiated the muscimol-induced inhibition of high K+-evoked release of [3H]GABA.
Negative_regulation (inhibition) of Localization (release) of GABA associated with gaba
20) Confidence 0.33 Published 1988 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2834538 Disease Relevance 0 Pain Relevance 0.55

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