INT29047

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Context Info
Confidence 0.08
First Reported 1987
Last Reported 2008
Negated 0
Speculated 0
Reported most in Abstract
Documents 18
Total Number 20
Disease Relevance 9.60
Pain Relevance 11.12

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

cytoplasm (Etf1)
Anatomy Link Frequency
cortex 2
brain 1
nervous system 1
hippocampus 1
cerebellum 1
Etf1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 296 100.00 Very High Very High Very High
Neurotransmitter 31 100.00 Very High Very High Very High
Calcitonin gene-related peptide 24 100.00 Very High Very High Very High
Opioid 10 99.92 Very High Very High Very High
Triptan 4 99.80 Very High Very High Very High
Clonidine 8 99.70 Very High Very High Very High
mu opioid receptor 5 99.68 Very High Very High Very High
Adelta 4 99.60 Very High Very High Very High
dopamine receptor 6 99.42 Very High Very High Very High
dorsal root ganglion 497 99.36 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neuropathic Pain 133 99.82 Very High Very High Very High
Cluster Headache 4 99.72 Very High Very High Very High
Diabetes Mellitus 20 99.60 Very High Very High Very High
Ganglion Cysts 512 99.36 Very High Very High Very High
Increased Venous Pressure Under Development 6 98.70 Very High Very High Very High
Nerve Compression Syndromes 315 98.00 Very High Very High Very High
Headache 6 97.84 Very High Very High Very High
Cognitive Disorder 33 94.08 High High
Nervous System Injury 28 92.72 High High
Attention Deficit Hyperactivity Disorder 90 89.32 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Taken together, these results suggest that MeHg induces release of DA via transporter-dependent, calcium- and vesicular-independent mechanism and it decreases the KCl-evoked DA release.
Negative_regulation (decreases) of release associated with dopamine
1) Confidence 0.08 Published 2002 Journal Neurochem. Int. Section Abstract Doc Link 11821154 Disease Relevance 0 Pain Relevance 0.72
Release inhibition may be associated with receptor downregulation in NTS regions associated with cardiovascular reflex transmission.
Negative_regulation (inhibition) of Release
2) Confidence 0.04 Published 1995 Journal Pharmacology Section Abstract Doc Link 8966194 Disease Relevance 0.61 Pain Relevance 0.31
Clonidine (0.1 mumol/l) reduced S2-evoked release in both normal (-30%) and diabetic (-44%) slices, but the groups were not different from each other.
Negative_regulation (reduced) of release associated with diabetes mellitus and clonidine
3) Confidence 0.03 Published 1995 Journal Pharmacology Section Abstract Doc Link 8966194 Disease Relevance 0.71 Pain Relevance 0.37
These results support the hypothesis that one important action of antimigraine drugs is the inhibition of CGRP release and that Adelta-fibres may play an important role in migraine pathogenesis.
Negative_regulation (inhibition) of release associated with cluster headache, migraine, adelta and calcitonin gene-related peptide
4) Confidence 0.02 Published 2001 Journal Eur. J. Neurosci. Section Abstract Doc Link 11422450 Disease Relevance 0.59 Pain Relevance 0.97
Previous studies suggest that calcitonin gene-related peptide (CGRP) released from Adelta-fibres plays a more important role than substance P (SP) released from C-fibres in inducing dural vasodilatation and that one of the antimigraine mechanisms of triptan drugs is inhibiting CGRP release.
Negative_regulation (inhibiting) of release associated with cluster headache, c fibre, adelta, triptan, increased venous pressure under development, substance p and calcitonin gene-related peptide
5) Confidence 0.02 Published 2001 Journal Eur. J. Neurosci. Section Abstract Doc Link 11422450 Disease Relevance 0.77 Pain Relevance 1.30
In rat cortex, DAGO induced a similar inhibition of release to that seen in guinea pig cortex, but DPDPE and U50,488H were much less effective, producing only weak inhibition even in large doses.
Negative_regulation (inhibition) of release in cortex
6) Confidence 0.01 Published 1987 Journal Neuropharmacology Section Abstract Doc Link 2821438 Disease Relevance 0 Pain Relevance 0.71
Stimulated release of [3H]NE from slices of cortex of the guinea pig and rat was inhibited by the mu opioid receptor agonist, Tyr-D-Ala2-Gly-NMePhe-Gly-ol (DAGO) in a naloxone-reversible manner, although naloxone itself produced a measurable inhibitory effect in the absence of opioid agonist.
Negative_regulation (inhibited) of release in cortex associated with mu agonist, narcan, agonist and mu opioid receptor
7) Confidence 0.01 Published 1987 Journal Neuropharmacology Section Abstract Doc Link 2821438 Disease Relevance 0 Pain Relevance 0.55
In guinea pig tissues, agonists acting preferentially through mu, delta and kappa receptors were all active in inhibiting stimulated release of [3H]NE, but in hippocampus and cerebellum of the rat, only DAGO inhibited release while DPDPE and U50,488H either had no effect or potentiated the stimulated release.
Negative_regulation (inhibited) of release in cerebellum associated with agonist and hippocampus
8) Confidence 0.01 Published 1987 Journal Neuropharmacology Section Abstract Doc Link 2821438 Disease Relevance 0 Pain Relevance 0.73
The ability of opioids to inhibit the release of norepinephrine (NE) from slice preparations of brain has been tested.
Negative_regulation (inhibit) of release in brain associated with opioid
9) Confidence 0.01 Published 1987 Journal Neuropharmacology Section Abstract Doc Link 2821438 Disease Relevance 0 Pain Relevance 0.17
Selective blockade of A1Rs increased basal [ATP] and relieved the block of KCl-evoked ATP release.
Negative_regulation (block) of release
10) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2630978 Disease Relevance 1.08 Pain Relevance 0.77
These data support our hypothesis that blockade of evoked ATP release is caused by increased A1R activation.
Negative_regulation (blockade) of release
11) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2630978 Disease Relevance 0.98 Pain Relevance 0.41
An alternative that remains to be explored is that increased P2Y1 receptor activation also contributes to the neuropathy-induced blockade of KCl-evoked ATP release.
Negative_regulation (blockade) of release associated with neuropathic pain
12) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2630978 Disease Relevance 0.93 Pain Relevance 0.44
We found that basal extracellular [ATP] was increased while KCl-evoked ATP release was suppressed in the injured DRG.
Negative_regulation (suppressed) of release in DRG associated with dorsal root ganglion
13) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2630978 Disease Relevance 1.13 Pain Relevance 0.77
However, in the continuous presence of NCPA (n = 7 DRG, 4 rats), there was a significant decrease in both basal and KCl-evoked ATP release (Fig. 3A, B), suggesting functional modulation of ATP release by A1R activation.


Negative_regulation (decrease) of release associated with dorsal root ganglion
14) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2630978 Disease Relevance 1.29 Pain Relevance 0.61
Previously, we used in vivo microdialysis in trigeminal ganglia to show that large increases in extracellular ATP levels result in the apparent loss of KCl-evoked ATP release [6].
Negative_regulation (loss) of release in trigeminal ganglia
15) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2630978 Disease Relevance 0.32 Pain Relevance 0.27
A1R activation leads to decreased Ca2+ influx through VGCCs and subsequent decreases in evoked transmitter release in these and other peripheral or CNS neurons [36,66].
Negative_regulation (decreases) of release in neurons
16) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2630978 Disease Relevance 0.50 Pain Relevance 0.31
In their hypothesis of biphasic MPH action, Seeman and Madras [42, 43] suggest that therapeutic doses of MPH elevate tonic dopamine while inhibiting phasic transmitter release in subcortical structures, leading to reduced postsynaptic receptor stimulation and psychomotor activation in response to salient stimuli.
Negative_regulation (inhibiting) of release associated with dopamine
17) Confidence 0.01 Published 2008 Journal Current Neuropharmacology Section Abstract Doc Link PMC2701285 Disease Relevance 0.53 Pain Relevance 0.19
At higher MPH doses, the magnitude of the increase is argued to markedly raise both the resting level of extracellular dopamine and the pulsatile dopamine output, thereby causing widespread stimulation of postsynaptic dopamine receptors, overcoming the presynaptic inhibition of further neurotransmitter release, and triggering generalized stimulation of the nervous system (for a review see [42, 43]).


Negative_regulation (inhibition) of release in nervous system associated with neurotransmitter, dopamine and dopamine receptor
18) Confidence 0.01 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2701285 Disease Relevance 0.15 Pain Relevance 0.60
In turn, these autoreceptors might have initiated the relative reduction of stimulus-induced pulsatile transmitter release.
Negative_regulation (reduction) of release
19) Confidence 0.01 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2701285 Disease Relevance 0 Pain Relevance 0.18
In guinea pig tissues, agonists acting preferentially through mu, delta and kappa receptors were all active in inhibiting stimulated release of [3H]NE, but in hippocampus and cerebellum of the rat, only DAGO inhibited release while DPDPE and U50,488H either had no effect or potentiated the stimulated release.
Negative_regulation (inhibited) of release in hippocampus associated with agonist and hippocampus
20) Confidence 0.00 Published 1987 Journal Neuropharmacology Section Abstract Doc Link 2821438 Disease Relevance 0 Pain Relevance 0.73

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