INT19366

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Context Info
Confidence 0.50
First Reported 1988
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 33
Total Number 33
Disease Relevance 6.51
Pain Relevance 6.61

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

cytosol (Ca2) extracellular space (Ca2) lyase activity (Ca2)
response to stress (Ca2) cytoplasm (Ca2)
Anatomy Link Frequency
internal 4
external 4
gastrocnemius 2
muscle 2
nerve 2
Ca2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Endogenous opioid 37 100.00 Very High Very High Very High
Neurotransmitter 20 100.00 Very High Very High Very High
Glutamate 18 100.00 Very High Very High Very High
opiate 4 99.98 Very High Very High Very High
Clonidine 2 99.98 Very High Very High Very High
Kinase C 30 99.84 Very High Very High Very High
agonist 84 99.48 Very High Very High Very High
Desipramine 4 99.18 Very High Very High Very High
noradrenaline 19 98.60 Very High Very High Very High
antagonist 62 97.72 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hypoxia 1460 99.98 Very High Very High Very High
Targeted Disruption 13 99.88 Very High Very High Very High
Drug Induced Neurotoxicity 1 99.80 Very High Very High Very High
Bordatella Infection 21 99.76 Very High Very High Very High
Morphine Dependence 2 97.08 Very High Very High Very High
Alkalosis 20 96.68 Very High Very High Very High
Muscular Atrophy 2 93.40 High High
Substance Withdrawal Syndrome 1 91.00 High High
INFLAMMATION 92 89.40 High High
Diabetes Mellitus 76 87.12 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
While this might indicate that anoxia inhibits mitochondrial Ca2+ release, there are other possible explanations (see following text).


Negative_regulation (inhibits) of Localization (release) of Ca2 associated with hypoxia
1) Confidence 0.50 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.71 Pain Relevance 0
When we utilised the protonophore FCCP, known to cause mitochondrial depolarisation, we could clearly see a decrease of oscillatory Ca2+ release induced by low doses of UTP.
Negative_regulation (decrease) of Localization (release) of Ca2
2) Confidence 0.47 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0
The effect was suspected to be caused by selective inhibition of Ca2+ release from intracellular Ca2+ store sites by affecting post-receptor mechanisms of f-MLP.
Negative_regulation (inhibition) of Localization (release) of Ca2
3) Confidence 0.46 Published 1991 Journal Masui Section Abstract Doc Link 2051570 Disease Relevance 0 Pain Relevance 0.46
Chronic inhibition of intracellular Ca2+ release or protein kinase C activation significantly reduces the development of morphine dependence.
Negative_regulation (inhibition) of Localization (release) of Ca2 associated with addiction, kinase c and morphine
4) Confidence 0.42 Published 1996 Journal Eur. J. Pharmacol. Section Title Doc Link 8739205 Disease Relevance 0.26 Pain Relevance 0.74
The residual Ca2+-independent release was not blocked by the intracellular Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid acetoxymethyl ester (100 microM) suggesting that intracellular Ca2+ stores are not involved in this component of veratridine effect.
Negative_regulation (blocked) of Localization (release) of Ca2
5) Confidence 0.38 Published 2001 Journal Neuroscience Section Abstract Doc Link 11440807 Disease Relevance 0 Pain Relevance 0.30
The noradrenaline uptake blockers, desipramine (10 microM) and nisoxetine (10 microM), inhibited the external Ca2+-independent release by 50 and 46%, respectively, indicating that the release partly originates from the reversal of transporters (carrier-mediated release).
Negative_regulation (inhibited) of Localization (release) of Ca2 in external associated with desipramine and noradrenaline
6) Confidence 0.38 Published 2001 Journal Neuroscience Section Abstract Doc Link 11440807 Disease Relevance 0.05 Pain Relevance 0.31
Morphine (100 microM), but not fentanyl (1 microM), decreased the amount of Ca2+ released from intracellular stores in response to caffeine in intact cells, and it inhibited the rate of Ca2+ uptake in isolated sarcoplasmic reticulum vesicles.
Negative_regulation (decreased) of Localization (released) of Ca2 in vesicles
7) Confidence 0.38 Published 1998 Journal Anesthesiology Section Body Doc Link 9856730 Disease Relevance 0 Pain Relevance 0
The incubation of synaptosomes in the presence of (+/-)-kavain up to a concentration of 500 mumol/l affected neither basal [Ca2+]i nor spontaneous release of glutamate, but dose-dependently reduced both veratridine-elevated [Ca2+]i (IC50 = 63.2 mumol/l) and glutamate-release (IC500 = 116.4 mumol/l).
Negative_regulation (reduced) of Localization (release) of Ca2 associated with glutamate
8) Confidence 0.38 Published 1996 Journal Neuropharmacology Section Abstract Doc Link 8734487 Disease Relevance 0 Pain Relevance 0.33
These findings agree with the previously observed decreases in Ca2+ influx in nerve ending preparations and inhibition of ICa2+ following opiate treatment and suggest opiates reduce Ca2+-dependent neurotransmitter release by altering the Ca2+ channel receptor protein in an allosteric fashion.
Negative_regulation (reduce) of Localization (release) of Ca2 in nerve associated with neurotransmitter and opiate
9) Confidence 0.38 Published 1988 Journal Neurochem. Res. Section Abstract Doc Link 2853309 Disease Relevance 0 Pain Relevance 0.70
In conclusion, all these class I antiarrhythmic drugs inhibited Ca2+ entry through voltage- and receptor-gated channels as well as Ca2+ release from intracellular stores.
Negative_regulation (inhibited) of Localization (release) of Ca2
10) Confidence 0.37 Published 1997 Journal Gen. Pharmacol. Section Abstract Doc Link 9352299 Disease Relevance 0 Pain Relevance 0.30
15 min in anoxic aglycemia), profound disturbance of Ca2+ homeostasis with near complete failure of Ca2+ clearance by both SERCA and PMCA and complete depletion of the ER Ca2+ stores.
Negative_regulation (failure) of Localization (clearance) of Ca2
11) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.21 Pain Relevance 0.04
While this could be due to a direct inhibition of mitochondrial Ca2+ release, it is also possible that it is simply an indirect consequence of reduced cytosolic Ca2+ clearance via PMCA and SERCA.
Negative_regulation (inhibition) of Localization (release) of Ca2
12) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.38 Pain Relevance 0
Note that ryanodine did not deplete ER stores of Ca2+ (as evidenced by the observation that after removal of ryanodine, caffeine evoked a large rise in [Ca2+]i, Fig. 4D) but none the less reduced Ca2+ release in response to anoxia.


Negative_regulation (reduced) of Neg (none) Localization (release) of Ca2 associated with hypoxia
13) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.59 Pain Relevance 0
This inhibition of Ca2+ clearance may help explain why the actions of anoxia on [Ca2+]i are relatively sustained.
Negative_regulation (inhibition) of Localization (clearance) of Ca2 associated with hypoxia
14) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.39 Pain Relevance 0
We found that while raising external pH to 8.8 caused a 90% inhibition of Ca2+ clearance in Ca2+-containing medium, the effects of alkalinization in Ca2+-free medium were much less pronounced and significant Ca2+ clearance remained even when the SERCA was also inhibited (unpublished results).
Negative_regulation (inhibition) of Localization (clearance) of Ca2 in external
15) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.47 Pain Relevance 0
While this could be due to a direct inhibition of mitochondrial Ca2+ release, it is also possible that it is simply an indirect consequence of reduced cytosolic Ca2+ clearance via PMCA and SERCA.
Negative_regulation (reduced) of Localization (clearance) of Ca2
16) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.37 Pain Relevance 0
Anoxia also significantly reduced Ca2+ clearance via both the SERCA and PMCA and substantially slowed Ca2+ recycling from the mitochondrion (probably as a consequence of inhibition of SERCA and PMCA).
Negative_regulation (reduced) of Localization (clearance) of Ca2 associated with hypoxia
17) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.18 Pain Relevance 0
15 min in anoxic aglycemia), profound disturbance of Ca2+ homeostasis with near complete failure of Ca2+ clearance by both SERCA and PMCA and complete depletion of the ER Ca2+ stores.
Negative_regulation (depletion) of Localization (clearance) of Ca2
18) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.22 Pain Relevance 0.04
Under conditions of anoxic aglycemia, there was a biphasic and more profound elevation of [Ca2+]i, which was associated with complete ER Ca2+ store emptying and progressive, and eventually complete, inhibition of Ca2+ clearance by PMCA and SERCA.
Negative_regulation (inhibition) of Localization (clearance) of Ca2
19) Confidence 0.36 Published 2008 Journal Journal of Neurophysiology Section Abstract Doc Link PMC2493471 Disease Relevance 0.49 Pain Relevance 0
The latter observation suggests that the trigger for Ca2+ release (ICa) was not reduced, with the delayed peak of the Ca2+ transient likely due to the prolonged action potential duration.
Neg (not) Negative_regulation (reduced) of Localization (release) of Ca2 associated with action potential duration
20) Confidence 0.36 Published 2008 Journal Diabetes Section Body Doc Link PMC2494698 Disease Relevance 0.38 Pain Relevance 0.05

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