INT28510

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Context Info
Confidence 0.68
First Reported 1980
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 21
Total Number 23
Disease Relevance 6.75
Pain Relevance 14.27

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

isomerase activity (Gpi) carbohydrate metabolic process (Gpi) cytoplasm (Gpi)
cytosol (Gpi) extracellular space (Gpi) extracellular region (Gpi)
Anatomy Link Frequency
neurons 3
nucleus 2
entopeduncular nucleus 1
pons 1
striatum 1
Gpi (Rattus norvegicus)
Pain Link Frequency Relevance Heat
dopamine receptor 209 99.98 Very High Very High Very High
Opioid 76 99.84 Very High Very High Very High
withdrawal 43 99.82 Very High Very High Very High
tolerance 5 99.74 Very High Very High Very High
opiate 5 99.60 Very High Very High Very High
Locus ceruleus 15 99.28 Very High Very High Very High
Morphine 20 99.18 Very High Very High Very High
Nicotine 4 99.16 Very High Very High Very High
Dopamine 822 99.00 Very High Very High Very High
gABA 183 98.98 Very High Very High Very High
Disease Link Frequency Relevance Heat
Parkinson's Disease 246 100.00 Very High Very High Very High
Disease Progression 4 99.60 Very High Very High Very High
Opiate Addiction 34 99.54 Very High Very High Very High
Disease 344 96.24 Very High Very High Very High
Syndrome 6 93.76 High High
Drug Dependence 1 90.48 High High
Wheal 4 89.72 High High
Congenital Anomalies 18 88.44 High High
Targeted Disruption 18 85.60 High High
Dyskinesias 172 85.04 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Morphine inhibited phosphofructokinase (PFK) and stimulated phosphohexose isomerase (PHI) activities.
Positive_regulation (stimulated) of phosphohexose isomerase associated with morphine
1) Confidence 0.68 Published 1980 Journal J. Endocrinol. Section Abstract Doc Link 6447740 Disease Relevance 0 Pain Relevance 0.86
Morphine inhibited phosphofructokinase (PFK) and stimulated phosphohexose isomerase (PHI) activities.
Positive_regulation (stimulated) of PHI associated with morphine
2) Confidence 0.68 Published 1980 Journal J. Endocrinol. Section Abstract Doc Link 6447740 Disease Relevance 0 Pain Relevance 0.88
To examine a role for the medullary nucleus paragigantocellularis (PGi) in mediation of the symptomatology of opioid withdrawal, bilateral electrical stimulation of the PGi was performed in conscious, unrestrained, opioid naive (nondependent) rats.
Positive_regulation (stimulation) of PGi in nucleus associated with withdrawal and opioid
3) Confidence 0.41 Published 1999 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 9972693 Disease Relevance 0.46 Pain Relevance 0.77
Tolerance to repeated stimulation of the PGi did not develop following a series of 30-min runs of stimulation over 3.5 h.
Positive_regulation (stimulation) of PGi associated with tolerance
4) Confidence 0.41 Published 1999 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 9972693 Disease Relevance 0.53 Pain Relevance 1.19
The results indicate that activation of the PGi by electrical stimulation can elicit behaviors similar to those observed during opioid withdrawal.
Positive_regulation (activation) of PGi associated with withdrawal and opioid
5) Confidence 0.41 Published 1999 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 9972693 Disease Relevance 0.50 Pain Relevance 1.43
There was also significant enhancement of spontaneous activity of PGi neurons for 30 min following administration of naloxone (2 mg/kg; s.c.) in morphine-dependent rats as an opiate withdrawal-induced activation of PGi neurons.
Positive_regulation (activation) of PGi in neurons associated with narcan, opiate, withdrawal and morphine
6) Confidence 0.41 Published 1998 Journal Brain Res. Section Abstract Doc Link 9838050 Disease Relevance 0 Pain Relevance 1.25
Participation of the nucleus paragigantocellularis (PGi) in mediation of opioid withdrawal was examined in conscious, unrestrained, non-opioid-dependent rats, using electrical stimulation of the PGi.
Spec (examined) Positive_regulation (stimulation) of PGi in nucleus associated with withdrawal and opioid
7) Confidence 0.40 Published 2000 Journal J. Biomed. Sci. Section Abstract Doc Link 10810247 Disease Relevance 0.33 Pain Relevance 0.98
Activation of the PGi by electrical stimulation can elicit behaviors similar to those observed during opioid withdrawal.
Positive_regulation (Activation) of PGi associated with withdrawal and opioid
8) Confidence 0.40 Published 2000 Journal J. Biomed. Sci. Section Abstract Doc Link 10810247 Disease Relevance 0.38 Pain Relevance 1.60
It is suggested that the peripherally induced effect of nicotine on LC neurons is indirectly mediated via activation of the PGi.
Positive_regulation (activation) of PGi in neurons associated with locus ceruleus and nicotine
9) Confidence 0.29 Published 1989 Journal Neurosci. Lett. Section Abstract Doc Link 2771156 Disease Relevance 0 Pain Relevance 0.65
For instance, our primate studies have demonstrated that activation of D1LRs in GPi and SNr leads to an inhibition of firing, most likely explained through increased GABA release in these nuclei.
Positive_regulation (activation) of GPi associated with gaba
10) Confidence 0.29 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0 Pain Relevance 0.27
Comparably, increased levels in the GPi correlate with an increased firing frequency of GPi neurons (Bezard et al., 1999; Boraud et al., 2000, 2001).
Positive_regulation (increased) of GPi in neurons
11) Confidence 0.25 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2947938 Disease Relevance 0.41 Pain Relevance 0
Microdialysis studies have, in fact, directly shown that GABA levels in the entopeduncular nucleus (in rats) or GPi (in monkeys) increase in response to activation of D1LRs (Ferre et al., 1996; Kliem et al., 2007a), and that GABA release is reduced upon D1LR antagonist administration (Floran et al., 1990).
Positive_regulation (increase) of GPi in entopeduncular nucleus associated with gaba and antagonist
12) Confidence 0.25 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0.06 Pain Relevance 0.51
In our recent experiments in monkeys, local activation of D2LRs in the GPi also resulted in decreased firing rates (Hadipour Niktarash et al., 2008), and blockade of these receptors increased firing rates (unpublished observations).
Positive_regulation (activation) of GPi
13) Confidence 0.25 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0.18 Pain Relevance 0.23
In confirmation of previous work, electrical stimulation of the PGi in opioid-nai;ve rats induced stimulus-intensity-related, withdrawal-like behaviors similar to those observed during naloxone-precipitated withdrawal from dependence upon butorphanol.
Positive_regulation (stimulation) of PGi associated with addiction, butorphanol, narcan, withdrawal and opioid
14) Confidence 0.19 Published 2002 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 12376173 Disease Relevance 0.09 Pain Relevance 1.42
Disease progression is associated with increasing metabolism in the STN and GPi, as well as in the dorsal pons and primary motor cortex.
Positive_regulation (increasing) of GPi in primary motor cortex associated with disease progression
15) Confidence 0.18 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2947938 Disease Relevance 0.98 Pain Relevance 0.32
In the GPi of MPTP-treated monkeys, i.e., the main output structure, the expression of GAD67 and GAD65 mRNAs is increased (Pedneault and Soghomonian, 1994; Soghomonian et al., 1994; Herrero et al., 1996).
Positive_regulation (increased) of GPi associated with parkinson's disease
16) Confidence 0.17 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2947938 Disease Relevance 0.85 Pain Relevance 0.06
The view that D1LR and D2LR effects are in some sense similar is obviously simplistic, but it may result in the recognition of overall response patterns of neurons in these nuclei to endogenous dopamine: the activity of GPe and STN neurons appears to be increased, while the activity of the basal ganglia output nuclei, GPi and SNr, appears to be reduced.
Positive_regulation (increased) of GPi in basal ganglia associated with dopamine
17) Confidence 0.17 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0.23 Pain Relevance 0.40
Activation of postsynaptic D5-receptors and subsequent activation of GPi cells may also occur, counteracting some of the changes in GABA release induced by presynaptic D1LR activation.
Positive_regulation (activation) of GPi associated with gaba
18) Confidence 0.17 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0.12 Pain Relevance 0.44
Overall, dopamine appears to decrease the neuronal activity in the GPi, likely via activation of D1LRs (Table 2).
Positive_regulation (activation) of GPi in neuronal associated with dopamine
19) Confidence 0.17 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0.09 Pain Relevance 0.26
Very few studies have examined the behavioral effects of dopamine receptor activation in the GPi.
Spec (examined) Positive_regulation (activation) of GPi associated with dopamine receptor
20) Confidence 0.17 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0.29 Pain Relevance 0.44

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