INT7832

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Context Info
Confidence 0.81
First Reported 1988
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 39
Total Number 41
Disease Relevance 6.81
Pain Relevance 26.54

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

extracellular space (Cck) extracellular region (Cck) DNA binding (Cck)
Anatomy Link Frequency
brain 4
spinal cord 2
PVN 2
gut 2
central nervous system 2
Cck (Mus musculus)
Pain Link Frequency Relevance Heat
Cholecystokinin 700 100.00 Very High Very High Very High
Enkephalin 50 100.00 Very High Very High Very High
Opioid 28 100.00 Very High Very High Very High
Neuropeptide 27 100.00 Very High Very High Very High
Neurotransmitter 14 100.00 Very High Very High Very High
gABA 3 100.00 Very High Very High Very High
Calcitonin gene-related peptide 3 100.00 Very High Very High Very High
Cannabinoid 11 99.80 Very High Very High Very High
Delta opioid receptors 6 99.78 Very High Very High Very High
Hyperalgesia 2 99.76 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hyperalgesia 2 99.76 Very High Very High Very High
Increased Venous Pressure Under Development 3 99.74 Very High Very High Very High
Gallstones 8 98.16 Very High Very High Very High
Anxiety Disorder 12 97.80 Very High Very High Very High
INFLAMMATION 32 93.64 High High
Pancreatitis 5 91.80 High High
Depression 13 87.88 High High
Drug Dependence 2 87.20 High High
Nutritional Deficiencies 44 84.92 Quite High
Stress 7 84.36 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results indicate that endogenous opiates are involved at peripheral levels in the regulation of gastric emptying of fat meals only and that such regulation involves release of CCK.
Localization (release) of CCK in fat associated with opiate and cholecystokinin
1) Confidence 0.81 Published 1988 Journal Am. J. Physiol. Section Abstract Doc Link 3407774 Disease Relevance 0 Pain Relevance 0.59
This hypothesis is related to recent evidence showing a cellular colocalization of neuropeptide CCK and cannabinoid type 1 (CB(1)) receptors in many central nervous system structures.
Localization (colocalization) of CCK in central nervous system associated with cannabinoid, neuropeptide, central nervous system and cholecystokinin
2) Confidence 0.79 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18412633 Disease Relevance 0.23 Pain Relevance 1.57
Recent studies have demonstrated that endocannabinoids can function as retrograde messengers, modulating the release of different neurotransmitters, including opioids, gamma-aminobutyric acid (GABA), and cholecystokinin (CCK), which could explain some of the responses observed after the stimulation of the CB1 cannabinoid receptor.
Localization (release) of cholecystokinin associated with endocannabinoid, gaba, neurotransmitter, cannabinoid receptor, cholecystokinin and opioid
3) Confidence 0.79 Published 2005 Journal Handb Exp Pharmacol Section Abstract Doc Link 16596773 Disease Relevance 0.72 Pain Relevance 0.85
Recent studies have demonstrated that endocannabinoids can function as retrograde messengers, modulating the release of different neurotransmitters, including opioids, gamma-aminobutyric acid (GABA), and cholecystokinin (CCK), which could explain some of the responses observed after the stimulation of the CB1 cannabinoid receptor.
Localization (release) of CCK associated with endocannabinoid, gaba, neurotransmitter, cannabinoid receptor, cholecystokinin and opioid
4) Confidence 0.79 Published 2005 Journal Handb Exp Pharmacol Section Abstract Doc Link 16596773 Disease Relevance 0.72 Pain Relevance 0.85
Co-localization of CART peptide and CCK-A receptor in vagal afferent neurons suggested that CART peptide might take part in mediating satiety effects of cholecystokinin [23].
Localization (localization) of CCK in afferent neurons associated with cholecystokinin
5) Confidence 0.77 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2587474 Disease Relevance 0.28 Pain Relevance 0.88
Therefore in this study, it is supposed that synergistic co-operation of leptin and CCK was preserved in 17- hour fasted C57BL/6 mice despite lowered leptin level after fasting.
Localization (operation) of CCK associated with cholecystokinin
6) Confidence 0.71 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2587474 Disease Relevance 0 Pain Relevance 0.48
The post hoc test showed a significant effect (P < 0.01) of parallel administration of CCK-8 and CART peptide on the Fos activation of cells in NTS in comparison with all other groups of animals (Fig. 3a, d).
Localization (administration) of CCK-8 associated with medulla and cholecystokinin
7) Confidence 0.71 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2587474 Disease Relevance 0 Pain Relevance 0.55
Experiment 1 Individual and combined administration of CCK-8 and CART(61-102)
Localization (administration) of CCK-8 associated with cholecystokinin
8) Confidence 0.71 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2587474 Disease Relevance 0 Pain Relevance 0.14
These neuronal cells are derived from an Atoh1-dependent lineage and likely use cholecystokinin (CCK) as a neurotransmitter or neuromodulator.
Localization (use) of CCK in neuronal associated with neurotransmitter and cholecystokinin
9) Confidence 0.71 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978708 Disease Relevance 0.07 Pain Relevance 0.42
The anti-analgesic effect of APGPR may be mediated by CCK release, since APGPR does not have affinity for CCK receptors.
Localization (release) of CCK associated with analgesic
10) Confidence 0.71 Published 2008 Journal Peptides Section Abstract Doc Link 18304696 Disease Relevance 0.08 Pain Relevance 0.70
Previous work indicates that the antianalgesic action of pentobarbital and neurotensin administered intracerebroventricularly in mice arises from activation of a descending system to release cholecystokinin (CCK) in the spinal cord where CCK is known to antagonize morphine analgesia.
Localization (release) of CCK in spinal cord associated with cholecystokinin, analgesia, morphine and spinal cord
11) Confidence 0.71 Published 1999 Journal Proc. Soc. Exp. Biol. Med. Section Abstract Doc Link 10193446 Disease Relevance 0 Pain Relevance 0.99
Previous work indicates that the antianalgesic action of pentobarbital and neurotensin administered intracerebroventricularly in mice arises from activation of a descending system to release cholecystokinin (CCK) in the spinal cord where CCK is known to antagonize morphine analgesia.
Localization (release) of cholecystokinin in spinal cord associated with cholecystokinin, analgesia, morphine and spinal cord
12) Confidence 0.71 Published 1999 Journal Proc. Soc. Exp. Biol. Med. Section Abstract Doc Link 10193446 Disease Relevance 0 Pain Relevance 0.98
In this work we have shown, by in vivo binding experiments, that the endogenous enkephalins, protected from degrading enzymes by mixed inhibitors such as kelatorphan and N-[(R,S)-2-benzyl-3-[(S)-2-amino-4-methylthiobutyldithio]-1-oxo pro pyl]- L-phenylalanine benzyl ester (RB 101), a systemically active prodrug, modulate CCK release in mouse brain, leading to an overall increase in the extracellular levels of CCK.
Localization (release) of CCK in brain associated with enkephalin and cholecystokinin
13) Confidence 0.71 Published 1992 Journal J. Neurochem. Section Abstract Doc Link 1357099 Disease Relevance 0 Pain Relevance 0.69
The specific binding of [3H]pBC 264 was also inhibited (25%) by intravenous injection of the selective delta-opioid agonist H-Tyr-D-Cys(StBu)-Gly-Phe-Leu-Thr(OtBu)-OH (BUBUC; 2 mg/kg) but not by the mu-agonist H-Tyr-D-Ala-Gly-(N-Me)Phe-Gly-ol (5 mg/kg), suggesting a preferential involvement of delta-opioid receptors in the modulation of CCK release.
Localization (release) of CCK associated with mu agonist, agonist, delta opioid receptors and cholecystokinin
14) Confidence 0.71 Published 1992 Journal J. Neurochem. Section Abstract Doc Link 1357099 Disease Relevance 0 Pain Relevance 0.94
Intracerebral injection of neurotensin into specific brain loci in rats produces hyperalgesia due to the release of cholecystokinin (CCK) in the spinal cord.
Localization (release) of cholecystokinin in brain associated with hyperalgesia, cholecystokinin and spinal cord
15) Confidence 0.68 Published 1999 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 10202849 Disease Relevance 0.10 Pain Relevance 0.74
Intracerebral injection of neurotensin into specific brain loci in rats produces hyperalgesia due to the release of cholecystokinin (CCK) in the spinal cord.
Localization (release) of CCK in brain associated with hyperalgesia, cholecystokinin and spinal cord
16) Confidence 0.68 Published 1999 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 10202849 Disease Relevance 0.10 Pain Relevance 0.74
The group of ß-gal+ cells in this hindbrain area was localized within a region of CCK immunoreactivity and some, but not all, ß-gal+ cells appeared to express CCK (Fig. 5B).
Localization (localized) of CCK in hindbrain associated with cholecystokinin
17) Confidence 0.67 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978708 Disease Relevance 0 Pain Relevance 0.35
Recent studies have also demonstrated that the endocannabinoids can function as retrograde messengers, modulating the release of different neurotransmitter, including opioids, GABA and cholecystokinin that have been classically involved in the control of anxiety-like responses.
Localization (release) of cholecystokinin associated with endocannabinoid, gaba, neurotransmitter, anxiety disorder, cholecystokinin and opioid
18) Confidence 0.66 Published 2005 Journal Curr. Pharm. Des. Section Abstract Doc Link 16250845 Disease Relevance 0.43 Pain Relevance 0.64
Dynorphin A(1-17) given intrathecally releases spinal cholecystokinin to produce an antianalgesic action against spinal morphine in the tail-flick test in CD-1 mice.
Localization (releases) of cholecystokinin in spinal associated with dynorphin, tail-flick, cholecystokinin and morphine
19) Confidence 0.64 Published 2001 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 11303046 Disease Relevance 0 Pain Relevance 1.17
The number of Fos immunoreactive cells distinctly increased after i.p. application of CCK-8 (0.4 ?
Localization (application) of CCK-8 associated with cholecystokinin
20) Confidence 0.62 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2587474 Disease Relevance 0 Pain Relevance 0.55

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