INT6417

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Context Info
Confidence 0.51
First Reported 1983
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 49
Total Number 49
Disease Relevance 19.60
Pain Relevance 36.81

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 5
brain 3
cortex 3
muscles 2
central nervous system 2
ABAT (Homo sapiens)
Pain Link Frequency Relevance Heat
gABA 1310 100.00 Very High Very High Very High
Central nervous system 192 100.00 Very High Very High Very High
Gabapentin 111 100.00 Very High Very High Very High
GABA receptor 30 100.00 Very High Very High Very High
opiate 21 100.00 Very High Very High Very High
Glutamate 80 99.98 Very High Very High Very High
Nicotine 12 99.98 Very High Very High Very High
Enkephalin 12 99.96 Very High Very High Very High
central pain 200 99.90 Very High Very High Very High
Dopamine 125 99.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Generalized Anxiety Disorder 36 100.00 Very High Very High Very High
Brain Injury 14 99.96 Very High Very High Very High
Tinnitus 6 99.92 Very High Very High Very High
Pain 301 99.90 Very High Very High Very High
Parkinson's Disease 18 99.70 Very High Very High Very High
Cramps 6 99.64 Very High Very High Very High
Panic Disorder 75 99.48 Very High Very High Very High
Schizophrenia 228 99.28 Very High Very High Very High
Aging 40 99.28 Very High Very High Very High
Adenocarcinoma 4 99.12 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Also, gabapentin has not been identified as a GABA reuptake inhibitor, and it is not converted to a GABA agonist.15,17 Gabapentin is a ligand of the ?
Negative_regulation (inhibitor) of GABA associated with gaba, agonist and gabapentin
1) Confidence 0.51 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2987504 Disease Relevance 0.33 Pain Relevance 1.24
Since destruction of the first or second order excitatory neurons produces analgesia, then it seems plausible that destruction of the third order neurons produces central pain because these neurons are net inhibitory and there is a deficiency of GABA or increase in the glutamate: GABA ratio.
Negative_regulation (deficiency) of GABA in neurons associated with pain, central pain, glutamate, gaba and analgesia
2) Confidence 0.46 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.68 Pain Relevance 2.03
Systemic administration of GABA-agonists, GABA uptake blockers and inhibitors of GABA-alpha-oxoglutarate transaminase (GABA-T) can produce potent analgesic actions in experimental animals and in man.
Negative_regulation (inhibitors) of GABA-alpha-oxoglutarate transaminase associated with gaba, analgesic and agonist
3) Confidence 0.43 Published 1984 Journal Drug Alcohol Depend Section Abstract Doc Link 6096107 Disease Relevance 0.09 Pain Relevance 1.10
Systemic administration of GABA-agonists, GABA uptake blockers and inhibitors of GABA-alpha-oxoglutarate transaminase (GABA-T) can produce potent analgesic actions in experimental animals and in man.
Negative_regulation (inhibitors) of GABA associated with gaba, analgesic and agonist
4) Confidence 0.43 Published 1984 Journal Drug Alcohol Depend Section Abstract Doc Link 6096107 Disease Relevance 0.09 Pain Relevance 1.10
Like stimulation of a particular subclass of dopamine receptors in the anterodorsal region of the caudate nucleus, inhibition of the GABA receptors in the noted part of the globus pallidus resulted in orofacial dyskinesia, viz. tic-like contractions of the facial, eye and ear muscles, and tongue protrusions.
Negative_regulation (inhibition) of GABA in tongue associated with movement disorders, tics, gaba receptor and dopamine receptor
5) Confidence 0.43 Published 1989 Journal Neuroscience Section Abstract Doc Link 2561520 Disease Relevance 0.34 Pain Relevance 0.45
GVG is an antiepileptic that elevates brain GABA concentrations by inhibiting an enzyme, GABA transaminase, that breaks down the neurotransmitter.
Negative_regulation (inhibiting) of GABA in brain associated with neurotransmitter and gaba
6) Confidence 0.42 Published 2008 Journal Addiction Science & Clinical Practice Section Body Doc Link PMC2797110 Disease Relevance 0.09 Pain Relevance 1.20
Based on clinical observations, one hypothesis also supports the role of GABA deficiency in the etiology of central pain and is as follows: In the three neuron network of nocioceptive transmission, a destructive procedure, including cordotomy, rhizotomy, neurectomy, and neurolysis of first order neurons produces an initial analgesic response because it is likely that the net neuronal excitation and glutamate:GABA ratio has been reduced.
Negative_regulation (deficiency) of GABA in neurons associated with pain, central pain, glutamate, neurolysis, gaba and analgesic
7) Confidence 0.39 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.73 Pain Relevance 1.88
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 GABA associated with scotoma, gaba, analgesic, agonist and bioavailability
8) Confidence 0.39 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.78 Pain Relevance 1.21
Down-regulation of gamma-amino butyric acid (GABA), a major inhibitory neurotransmitter of the central auditory pathway, is a potential mechanism for the loss of inhibition.
Negative_regulation (Down-regulation) of GABA associated with neurotransmitter and gaba
9) Confidence 0.38 Published 2007 Journal Prog. Brain Res. Section Abstract Doc Link 17956793 Disease Relevance 0.44 Pain Relevance 0.26
Both animal studies and human clinical trials implicate loss of inhibition, and specifically loss of GABA function, in the development of acoustic trauma-induced tinnitus.
Negative_regulation (loss) of GABA associated with tinnitus, gaba and noise-induced hearing loss
10) Confidence 0.38 Published 2007 Journal Prog. Brain Res. Section Abstract Doc Link 17956793 Disease Relevance 0.51 Pain Relevance 0.25
Factors that augment activity in this pathway include modest increases in [K+]o; loss of GABA inhibition; short-term, frequency-dependent facilitation (frequencies of 1-2 Hz); feedback activation of kainate autoreceptors; and release of zinc from recurrent mossy fiber boutons.
Negative_regulation (inhibition) of GABA in boutons associated with gaba
11) Confidence 0.38 Published 2003 Journal Neurochem. Res. Section Abstract Doc Link 14584819 Disease Relevance 0.53 Pain Relevance 0.30
Muscle cramp as the result of impaired GABA function--an electrophysiological and pharmacological observation.
Negative_regulation (impaired) of GABA in Muscle associated with cramps and gaba
12) Confidence 0.38 Published 1993 Journal Muscle Nerve Section Title Doc Link 8413375 Disease Relevance 0.63 Pain Relevance 0.28
Also, these findings would support the GABA hypothesis of schizophrenia, which suggests that there is insufficient GABA inhibition of dopaminergic neurotransmission in patients with schizophrenia.34–36
Negative_regulation (inhibition) of GABA associated with gaba and schizophrenia
13) Confidence 0.38 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2987504 Disease Relevance 0.68 Pain Relevance 1.01
In addition to increasing cerebral levels of GABA and facilitating GABA neurotransmission (Kuzniecky et al., 1998), topiramate weakens the action of glutamate, a neurotransmitter that opposes GABA’s potentially therapeutic reduction of dopamine activity.
Negative_regulation (reduction) of GABA associated with dopamine, neurotransmitter, glutamate and gaba
14) Confidence 0.37 Published 2008 Journal Addiction Science & Clinical Practice Section Body Doc Link PMC2797110 Disease Relevance 0.46 Pain Relevance 0.86
The decrease in minute volume was mainly due to a decrease in tidal volume after GABA and muscimol, while GHBA reduced minute volume due to a decrease in respiratory frequency.
Negative_regulation (decrease) of GABA in respiratory associated with gaba
15) Confidence 0.36 Published 1983 Journal Biol. Neonate Section Abstract Doc Link 6407536 Disease Relevance 0 Pain Relevance 0.39
This paper hopes to spark interest in development of GABA ester analogs as novel analgesics for central pain and perhaps other conditions of the CNS where GABA deficiency is thought to exist.



Negative_regulation (deficiency) of GABA associated with pain, central pain, gaba, analgesic and central nervous system
16) Confidence 0.34 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.24 Pain Relevance 0.73
At physiologic pH, GABA exists as a zwitterion impermeable to the blood brain barrier, but selected GABA esters of ethanol, glucose, diethamino ethanol, dehydroascorbic acid, cholesterol, and inositol may cross the BBB and replace GABA in the CNS provided that central nervous system esterases can hydrolyze the prodrug.
Negative_regulation (replace) of GABA in blood associated with gaba and central nervous system
17) Confidence 0.34 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.23 Pain Relevance 0.78
This paper is not the first publication to link central pain and GABA deficiency and addresses a basic hypothesis without taking into account possible other neurotransmitters and collateral pathways.12,13 My hope is to present a potential therapy for the treatment of central pain, an intractable devastating condition, with selected GABA esters including special consideration to parallel pharmacologic properties with local ester anesthetics that may speed drug development.


Negative_regulation (deficiency) of GABA associated with pain, central pain, neurotransmitter and gaba
18) Confidence 0.34 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.66 Pain Relevance 1.70
Based on neurophysiology and neuropharmacology, devastating central pain caused by lesions of the inhibitory neurons of the thalamus and thalamocortical tracts probably produces GABA deficiency.
Negative_regulation (deficiency) of GABA in thalamus associated with pain, central pain, gaba and thalamus
19) Confidence 0.34 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.19 Pain Relevance 0.91
If post synaptic receptors are functional after brain injury, replenishing GABA may provide relief of symptoms.
Negative_regulation (replenishing) of GABA in brain associated with gaba and brain injury
20) Confidence 0.34 Published 2010 Journal Perspect Medicin Chem Section Body Doc Link PMC2918363 Disease Relevance 0.19 Pain Relevance 0.85

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