INT5359

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Context Info
Confidence 0.62
First Reported 1981
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 12
Total Number 12
Disease Relevance 5.11
Pain Relevance 8.54

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
brain 3
neurons 2
synapse 2
Abat (Rattus norvegicus)
Pain Link Frequency Relevance Heat
gABA 135 100.00 Very High Very High Very High
Enkephalin 6 99.92 Very High Very High Very High
GABAergic 7 99.50 Very High Very High Very High
local anesthetic 5 99.36 Very High Very High Very High
agonist 11 99.18 Very High Very High Very High
Morphine 4 97.84 Very High Very High Very High
GABA receptor 7 97.20 Very High Very High Very High
pregabalin 153 96.66 Very High Very High Very High
Glutamate receptor 7 96.16 Very High Very High Very High
Glutamate 50 96.04 Very High Very High Very High
Disease Link Frequency Relevance Heat
Decapitation 2 98.32 Very High Very High Very High
Urological Neuroanatomy 6 97.80 Very High Very High Very High
Syndrome 286 96.72 Very High Very High Very High
Convulsion 383 94.64 High High
Epilepsy 224 89.72 High High
Headache 81 89.04 High High
Generalized Anxiety Disorder 7 88.40 High High
Cluster Headache 6 86.36 High High
Stress 7 85.16 High High
Body Weight 4 84.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In particular, pregabalin does not bind to GABAA, GABAB or benzodiazepine receptors and is neither metabolically converted to GABA or to a GABA agonist, nor it has any effect on the uptake or degradation of GABA (Errante and Petroff 2002; Ben-Menachem 2004).
Protein_catabolism (degradation) of GABA associated with pregabalin, gaba and agonist
1) Confidence 0.62 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2646650 Disease Relevance 0.85 Pain Relevance 1.45
The in vivo turnover of GABA in the brain was estimated by taking advantages of the postmortem accumulation of GABA following decapitation and of the selective inhibitory action of a low dose of aminooxyacetic acid on the GABA degrading system, respectively.
Protein_catabolism (degrading) of GABA in brain associated with gaba and decapitation
2) Confidence 0.57 Published 1983 Journal J. Neurochem. Section Abstract Doc Link 6130124 Disease Relevance 0.39 Pain Relevance 0.58
The effects of local anesthetics on the synthesis, release, and degradation of gamma-aminobutyric acid (GABA) in rat brains were investigated.
Protein_catabolism (degradation) of GABA in brains associated with gaba and local anesthetic
3) Confidence 0.56 Published 1983 Journal Anesthesiology Section Abstract Doc Link 6859579 Disease Relevance 0.17 Pain Relevance 0.68
Although the possibility that GBL inhibits GABA degradation is not excluded, the compound appears to increase the sensitivity of GABA receptor to GABA mimetics in the gastric acid secretion.
Protein_catabolism (degradation) of GABA associated with gaba and gaba receptor
4) Confidence 0.56 Published 1983 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 6668764 Disease Relevance 0 Pain Relevance 0.83
These changes manifested themselves in activation of GABA degradation with simultaneous rise of the succinate--but not isocitrate dehydrogenase activity, inhibition of glutamate dehydrogenase activity and worsening of blood supply to neurons.
Protein_catabolism (degradation) of GABA in neurons associated with glutamate and gaba
5) Confidence 0.54 Published 1992 Journal Patol Fiziol Eksp Ter Section Abstract Doc Link 1303507 Disease Relevance 0.41 Pain Relevance 0.49
The inhibitory action of DPA on GABA degradation, resulting in an enhanced release of GABA, is probably responsible for this behavioral effect, since GABA antagonists, like bicuculline and picrotoxin, have been shown to suppress this behavior.
Protein_catabolism (degradation) of GABA associated with gaba and antagonist
6) Confidence 0.52 Published 1981 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 6791219 Disease Relevance 0.10 Pain Relevance 0.51
Results show that there is long-term survival and stability of GABA, enkephalin and NADPH-d cell populations in the grafts and that some grafted spiny neurons may exhibit altered phenotype from those of host striatum.
Protein_catabolism (stability) of GABA in neurons associated with gaba and enkephalin
7) Confidence 0.45 Published 1990 Journal Brain Res. Section Abstract Doc Link 1980852 Disease Relevance 0 Pain Relevance 0.53
Attempts to categorize AED according to their molecular targets have generally assigned them to three main groups; those that block voltage gated ion channels (Na and Ca), and those that either enhance GABAergic inhibition (by altering GABA synthesis/breakdown or potentiating GABAA-receptor (GABAAr) activity) or reduce glutamatergic excitation (blocking glutamate receptors, reducing glutamate release) (e.g.
Protein_catabolism (breakdown) of GABA associated with glutamate, gaba, glutamate receptor, gabaergic and antiepileptic drug
8) Confidence 0.26 Published 2010 Journal Neuroscience Section Body Doc Link PMC2877872 Disease Relevance 0.07 Pain Relevance 0.43
In addition it does not augment GABAA responses in cultured neurons, alter rat brain GABA concentration or have acute effects on GABA uptake or degradation.
Protein_catabolism (degradation) of GABA in brain associated with gaba
9) Confidence 0.22 Published 2009 Journal Psychiatry Investigation Section Body Doc Link PMC2796047 Disease Relevance 0.16 Pain Relevance 1.12
VGB’s main actions are on the GABA-ergic synapse as an irreversible inhibitor of the GABA-degrading enzyme, GABA transaminase.
Protein_catabolism (degrading) of GABA in synapse associated with gaba
10) Confidence 0.11 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2646636 Disease Relevance 1.04 Pain Relevance 0.26
VGB’s main actions are on the GABA-ergic synapse as an irreversible inhibitor of the GABA-degrading enzyme, GABA transaminase.
Protein_catabolism (degrading) of GABA transaminase in synapse associated with gaba
11) Confidence 0.11 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2646636 Disease Relevance 1.05 Pain Relevance 0.26
Valproate is provided with two mechanisms of action, being able to inhibit GABA-transaminase, which causes GABA degradation and, at the same time, to activate glutamic - decarboxylase, that induces GABA synthesis.
Protein_catabolism (degradation) of GABA associated with gaba
12) Confidence 0.10 Published 2009 Journal The Open Neurology Journal Section Body Doc Link PMC2771268 Disease Relevance 0.87 Pain Relevance 1.40

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