INT155989

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Context Info
Confidence 0.38
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 1.29
Pain Relevance 6.95

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
pyramidal cells 2
DA neurons 2
neurons 2
ABAT (Homo sapiens)
Pain Link Frequency Relevance Heat
gABA 115 100.00 Very High Very High Very High
Glutamate 41 100.00 Very High Very High Very High
Cannabinoid 69 99.70 Very High Very High Very High
Pyramidal cell 2 99.68 Very High Very High Very High
pregabalin 10 99.62 Very High Very High Very High
Dopamine 178 99.52 Very High Very High Very High
Gabapentin 10 99.32 Very High Very High Very High
anticonvulsant 8 99.18 Very High Very High Very High
Opioid 58 98.88 Very High Very High Very High
Substantia nigra 14 98.50 Very High Very High Very High
Disease Link Frequency Relevance Heat
Scotoma 1 98.76 Very High Very High Very High
Pain 86 92.32 High High
Disease 91 84.56 Quite High
Toxicity 2 80.40 Quite High
Anxiety Disorder 7 77.80 Quite High
Schizophrenia 119 60.00 Quite High
Xerostomia 1 59.52 Quite High
Heart Rate Under Development 1 58.92 Quite High
Pressure Volume 2 Under Development 2 58.40 Quite High
Cannabis Dependence 24 57.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
For example, vigabatrin, a GABA agonist with good bioavailability and analgesic action, produced visual field defects in 1/3 of patients during therapy and tiagabine, a selective inhibitor of GABA transport (GAT1), took twenty years to bring to market.17,18
Negative_regulation (inhibitor) of Localization (transport) of GABA associated with scotoma, gaba, analgesic, agonist and bioavailability
1) Confidence 0.38 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.78 Pain Relevance 1.22
An anticonvulsant mode of action of both drugs may be the reduction of a proconvulsant exocytotic GABA release.
Negative_regulation (reduction) of Localization (release) of GABA associated with gaba and anticonvulsant
2) Confidence 0.37 Published 2009 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 19002437 Disease Relevance 0.05 Pain Relevance 1.35
When a GABA transport inhibitor was present throughout superfusion to isolate exocytotic conditions, gabapentin and pregabalin (100 microM each) reduced K(+)-evoked (3)H-GABA release by 39% and 47%, respectively.
Negative_regulation (reduced) of Localization (release) of GABA associated with pregabalin, gaba and gabapentin
3) Confidence 0.27 Published 2009 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 19002437 Disease Relevance 0.08 Pain Relevance 1.43
In the rodent hippocampus, a specific class of GABAergic interneurons was detected to express CB1Rs, and moreover, endogenous and exogenous cannabinoids were shown to inhibit GABA release in CA1 pyramidal cells (Hoffman and Lupica 2000; Katona et al. 1999, 2000) and pyramidal cells of the ventral tegmental area (Pistis et al. 2001).
Negative_regulation (inhibit) of Localization (release) of GABA in pyramidal cells associated with ventral tegmentum, gaba, pyramidal cell, cannabinoid, gabaergic and hippocampus
4) Confidence 0.08 Published 2009 Journal Psychopharmacology (Berl) Section Body Doc Link PMC2806533 Disease Relevance 0.17 Pain Relevance 0.82
It has been observed that opioids act indirectly to excite neurons through a presynaptic inhibition of GABA release, so-called disinhibition.
Negative_regulation (inhibition) of Localization (release) of GABA in neurons associated with gaba and opioid
5) Confidence 0.04 Published 2008 Journal Brain Section Body Doc Link PMC2367693 Disease Relevance 0 Pain Relevance 0.91
eCBs, released upon depolarization and/or receptor activation, can transiently affect synaptic efficacy by suppressing either GABA or glutamate release, thus provoking depolarization-induced suppression of inhibition (DSI) or excitation (DSE), respectively [1, 31, 48, 216]. eCBs can also affect other forms of short term synaptic transmission, which are induced by more physiologically relevant patterns of synaptic activity [15, 17, 136], and result in modulation of synaptic strength and/or firing pattern in vivo [10, 29, 136].
Negative_regulation (suppressing) of Localization (release) of GABA associated with glutamate and gaba
6) Confidence 0.03 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.16 Pain Relevance 0.49
Activation of CB1 or TRPV1 receptors in the SN exerts opposing actions on synaptic afferent to DA neurons, CB1 receptors inhibit glutamate and GABA release, whereas TRPV1 receptors potentiate excitatory transmission, possibly by depolarization of axon terminals and Ca2+ entry [127].
Negative_regulation (inhibit) of Localization (release) of GABA in DA neurons associated with gaba, glutamate, dopamine and substantia nigra
7) Confidence 0.03 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.05 Pain Relevance 0.73

General Comments

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