INT9027

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Context Info
Confidence 0.66
First Reported 1982
Last Reported 2010
Negated 5
Speculated 1
Reported most in Abstract
Documents 24
Total Number 25
Disease Relevance 6.04
Pain Relevance 10.19

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

lyase activity (Ddc) intracellular (Ddc) cellular amino acid metabolic process (Ddc)
cytoplasm (Ddc)
Anatomy Link Frequency
plasma 3
striatum 3
substantia nigra 1
RVLM 1
neurons 1
Ddc (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Bioavailability 36 99.96 Very High Very High Very High
Dopamine 217 99.84 Very High Very High Very High
Enkephalin 14 99.74 Very High Very High Very High
Rostral ventrolateral medulla 5 99.68 Very High Very High Very High
antagonist 59 99.58 Very High Very High Very High
Catecholamine 32 99.44 Very High Very High Very High
Central nervous system 18 99.04 Very High Very High Very High
Substantia nigra 63 98.84 Very High Very High Very High
nMDA receptor 122 98.46 Very High Very High Very High
Dynorphin 4 98.32 Very High Very High Very High
Disease Link Frequency Relevance Heat
Dyskinesias 102 99.64 Very High Very High Very High
Disease 281 99.00 Very High Very High Very High
Hypertension 4 98.08 Very High Very High Very High
Hypoxia 16 94.20 High High
Attention Deficit Hyperactivity Disorder 4 91.56 High High
Muscle Rigidity 4 91.08 High High
Alcohol Addiction 77 89.76 High High
Parkinsonian Disorders 6 88.56 High High
Hepatotoxicity 9 86.56 High High
Ganglion Cysts 12 86.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Sixty min pretreatment with the high affinity NMDA receptor-channel blockers MK 801 (0.01, 0.1 and 1 mg/kg) and phencyclidine (4 mg/kg) elevated AADC activity in both the CS and SN (2- to 3-fold).
Positive_regulation (elevated) of AADC associated with substantia nigra and nmda receptor
1) Confidence 0.66 Published 1998 Journal Brain Res. Section Abstract Doc Link 9593857 Disease Relevance 0 Pain Relevance 0.60
Similarly pronounced increases in AADC activity in CS (1.9-fold) and SN (2.8-fold) were detected after administering clonidine (2 mg/kg).
Positive_regulation (increases) of AADC associated with substantia nigra and clonidine
2) Confidence 0.66 Published 1998 Journal Brain Res. Section Abstract Doc Link 9593857 Disease Relevance 0 Pain Relevance 0.72
These experiments indicate that blocking the NMDA receptor-channel (and to a lesser extent the glycine site) or stimulating alpha2-adrenoceptors, profoundly increases AADC activity, more especially in the SN than CS.
Positive_regulation (increases) of AADC associated with substantia nigra and nmda receptor
3) Confidence 0.47 Published 1998 Journal Brain Res. Section Abstract Doc Link 9593857 Disease Relevance 0 Pain Relevance 0.68
The synthesis of 5-HT was assessed by measuring the accumulation of 5-hydroxytryptophan (5-HTP) after blockade of aromatic amino acid decarboxylase induced by m-hydroxybenzylhydrazine (NSD-1015), at 100 mg/kg i.p., 30 min before sacrifice.
Positive_regulation (induced) of aromatic amino acid decarboxylase
4) Confidence 0.42 Published 1999 Journal Eur Neuropsychopharmacol Section Abstract Doc Link 10647099 Disease Relevance 0.28 Pain Relevance 0.63
Administration of increasing doses of L-DOPA or L-5-HTP resulted in a dose-related decrease in neonatal survival time.
Positive_regulation (increasing) of L-DOPA
5) Confidence 0.41 Published 1982 Journal Acta Pharmacol Toxicol (Copenh) Section Abstract Doc Link 6980559 Disease Relevance 0.33 Pain Relevance 0.32
There was no significant difference in the basal concentrations of catecholamines between the lines, but the accumulation of L-DOPA was significantly greater in the ANA than the AA rats, suggesting differences in catecholamine turnover.
Positive_regulation (accumulation) of L-DOPA associated with catecholamine
6) Confidence 0.39 Published 1991 Journal Alcohol Section Abstract Doc Link 1829611 Disease Relevance 0.14 Pain Relevance 0.72
Even more striking increases in AADC were noted with 40 mg/kg amantadine (3.8-fold for CS, 9.0-fold for SN), 40 mg/kg memantine (3.4-fold for CS, 3.1-fold for SN; 20 mg/kg no effect) and 40 mg/kg dextromethorphan (3.4-fold for CS, 6.2-fold for SN, in 6/10 'responders').
Positive_regulation (increases) of AADC associated with substantia nigra and dextromethorphan
7) Confidence 0.38 Published 1998 Journal Brain Res. Section Abstract Doc Link 9593857 Disease Relevance 0 Pain Relevance 0.64
Impaired TTX-sensitive neuronal activity to release L-DOPA in the NTS and enhanced TTX-sensitive neuronal activity including a decrease in decarboxylation of L-DOPA to dopamine and an increase in sensitivity of the recognition site to L-DOPA in the RVLM are relevant to the maintenance of hypertension in spontaneously hypertensive rats.
Positive_regulation (increase) of L-DOPA in RVLM associated with tetrodotoxin, rostral ventrolateral medulla, dopamine and hypertension
8) Confidence 0.32 Published 1995 Journal Neurosci. Res. Section Abstract Doc Link 8532212 Disease Relevance 0.36 Pain Relevance 0.86
Dopa-decarboxylase activity remained unchanged.
Neg (unchanged) Positive_regulation (unchanged) of Dopa-decarboxylase
9) Confidence 0.26 Published 1982 Journal Eur. J. Pharmacol. Section Abstract Doc Link 6124436 Disease Relevance 0 Pain Relevance 0.40
Calcium-permeable AMPA receptors are involved in the induction and expression of l-DOPA-induced dyskinesia in Parkinson's disease.
Positive_regulation (induction) of l-DOPA associated with enkephalin, disease and dyskinesias
10) Confidence 0.24 Published 2010 Journal J. Neurochem. Section Title Doc Link 20456008 Disease Relevance 1.26 Pain Relevance 0.19
After oral administration of L-DOPA alone (at 20 mg/kg) or L-DOPA + carbidopa (at 20 + 5 mg/kg), there was a rather rapid, short-lasting increase in the plasma L-DOPA level (estimated plasma half-life of approximately 1 h) (Figure 4A).
Positive_regulation (increase) of L-DOPA in plasma
11) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916818 Disease Relevance 0 Pain Relevance 0.04
By contrast, only a very small increase (no statistical significance) in L-DOPA plasma concentrations was observed in these animals (Figure 5).
Positive_regulation (increase) of L-DOPA in plasma
12) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916818 Disease Relevance 0 Pain Relevance 0.07
The significant reduction of 3-OMD by EGCG may increase L-DOPA bioavailability in the central nervous system and particularly, reduce potential cytotoxicity associated with elevated levels of 3-OMD.
Positive_regulation (increase) of L-DOPA in central nervous system associated with central nervous system and bioavailability
13) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916818 Disease Relevance 0.38 Pain Relevance 0.24
The total dopamine level in rat striatum was not increased by treatment with L-DOPA alone but was slightly increased at 2 and 3 h after the combined L-DOPA + carbidopa treatment (Figure 4C).
Neg (not) Positive_regulation (increased) of L-DOPA in striatum associated with dopamine
14) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916818 Disease Relevance 0 Pain Relevance 0.05
Presently, tolcapone and entacapone are the two COMT inhibitors approved for clinical use for enhancement of therapeutic benefits of L-DOPA.
Positive_regulation (enhancement) of L-DOPA
15) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916818 Disease Relevance 0.27 Pain Relevance 0.14
Notably, our observation of a strong reduction of 3-OMD level but a lack of meaningful increase in L-DOPA plasma concentration in rats treated with L-DOPA + carbidopa + EGCG was similar to the earlier observations with tolcapone or entacapone in rats [28]–[31] or human subjects [32]–[34] that were also treated with L-DOPA + carbidopa.
Positive_regulation (increase) of L-DOPA in plasma
16) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916818 Disease Relevance 0 Pain Relevance 0.06
These data demonstrate that J-113397 and L-DOPA exert their antiparkinsonian action through overinhibition of nigrothalamic transmission and suggest that NOP receptor antagonists may be useful as an adjunct to L-DOPA therapy for Parkinson's disease.
Positive_regulation (adjunct) of L-DOPA associated with antagonist and disease
17) Confidence 0.10 Published 2007 Journal J. Neurosci. Section Abstract Doc Link 17287504 Disease Relevance 0.17 Pain Relevance 0.70
In the substantia nigra and corpus striatum of reserpine-treated rats, acute injection of memantine (40 mg/kg) strongly increased L-DOPA decarboxylase (DDC), whilst not affecting or decreasing 5- HTPDC activity [72].
Neg (not) Positive_regulation (increased) of L-DOPA in corpus striatum associated with substantia nigra
18) Confidence 0.05 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2645549 Disease Relevance 0.87 Pain Relevance 0.24
After subchronic L-DOPA, zif-268 mRNA labelling was still increased in the striatonigral pathway, limited to dynorphin(+) neurons, whereas in all other neurons it was similar to the control value.
Positive_regulation (increased) of L-DOPA in neurons associated with dynorphin
19) Confidence 0.04 Published 2005 Journal Eur. J. Neurosci. Section Abstract Doc Link 15813929 Disease Relevance 0 Pain Relevance 0.33
PreproTRH mRNA levels in the dopamine-depleted striatum of the L-DOPA-treated animals were positively correlated with the behavioral scores (Pearson's r ?
Positive_regulation (striatum) of L-DOPA in striatum associated with dopamine
20) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978093 Disease Relevance 0.14 Pain Relevance 0.17

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