INT29831

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Context Info
Confidence 0.26
First Reported 1988
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 2
Total Number 14
Disease Relevance 0.50
Pain Relevance 1.88

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

signal transduction (Gabbr2) plasma membrane (Gabbr2) cytoplasm (Gabbr2)
signal transducer activity (Gabbr2)
Anatomy Link Frequency
longitudinal muscle 1
neuron 1
Gabbr2 (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 149 100.00 Very High Very High Very High
Action potential 13 99.88 Very High Very High Very High
adenocard 1 97.70 Very High Very High Very High
tolerance 1 95.88 Very High Very High Very High
narcan 1 95.78 Very High Very High Very High
tetrodotoxin 13 95.24 Very High Very High Very High
withdrawal 2 95.20 Very High Very High Very High
Morphine 8 94.56 High High
Dopamine 13 90.56 High High
depression 117 86.88 High High
Disease Link Frequency Relevance Heat
Opiate Addiction 1 94.86 High High
Depression 117 86.88 High High
Adhesions 26 80.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The effect was evident also in ileal preparations from morphine-tolerant animals in which a withdrawal syndrome was induced by the administration of naloxone before sacrifice. 3) The phenomenon was specific since the dose-response curve of the adenosine-inhibitory effect was comparable in preparations from tolerant animals and controls. 4) The hyporesponsiveness to GABA-B receptor activation began 12 h after pellet implantation and was maximal on the third day. 5) It is concluded that during tolerance to and withdrawal from morphine there is a hyporesponsiveness of GABA-B receptors in "in vitro" guinea-pig ileal longitudinal muscle-myenteric plexus preparations.
Positive_regulation (activation) of GABA-B receptor in longitudinal muscle associated with gaba, adenocard, tolerance, narcan, withdrawal and morphine
1) Confidence 0.26 Published 1988 Journal Pharmacol Res Commun Section Abstract Doc Link 2845451 Disease Relevance 0.09 Pain Relevance 1.15
On the other hand, shortening the duration of coupled conditioning stimulation consisting of GABABR activation and the [Ca2+]i increase dramatically weakened the suppressive effect of GABABR activation on the CaMKII activation (Figure 3B–E; also see Supplementary Figure 3).
Positive_regulation (activation) of GABABR
2) Confidence 0.22 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, GABABR activation suppressed the sustained CaMKII activation, as suggested by our earlier experiments (Kawaguchi and Hirano, 2002).
Positive_regulation (activation) of GABABR
3) Confidence 0.22 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.04
Thus, the induction of RP depends predominantly on the intensity rather than the duration of [Ca2+]i increase, whereas its suppression depends more strongly on the duration than on the intensity of GABABR activation.
Positive_regulation (activation) of GABABR
4) Confidence 0.22 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
In any case, a transient [Ca2+]i increase caused sustained CaMKII activation, which was largely suppressed by simultaneous GABABR activation.
Positive_regulation (activation) of GABABR
5) Confidence 0.19 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
On the other hand, shortening the duration of coupled conditioning stimulation consisting of GABABR activation and the [Ca2+]i increase dramatically weakened the suppressive effect of GABABR activation on the CaMKII activation (Figure 3B–E; also see Supplementary Figure 3).
Positive_regulation (activation) of GABABR
6) Confidence 0.16 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, consistently with the simulation results, CaMKII was activated for a long time after brief depolarization of a Purkinje neuron, and this sustained activation was suppressed by GABABR activation during the depolarization.
Positive_regulation (activation) of GABABR in neuron
7) Confidence 0.15 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.11
We next examined the effect of GABABR activation coupled with a [Ca2+]i increase.
Spec (examined) Positive_regulation (activation) of GABABR
8) Confidence 0.15 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.05
The computational simulation showed that a transient [Ca2+]i increase induced long-term activation of CaMKII, which was suppressed by GABABR activation coupled with the [Ca2+]i increase.
Positive_regulation (activation) of GABABR
9) Confidence 0.15 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
As a result, GABABR activation is thought to counteract CaMKII activity and suppress RP induction (Kawaguchi and Hirano, 2000, 2002).
Positive_regulation (activation) of GABABR
10) Confidence 0.15 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.10
Using the simulation model, we first attempted to reproduce the earlier experimental findings that different combinations of [Ca2+]i increase and GABABR activation result in RP induction or suppression.
Positive_regulation (activation) of GABABR
11) Confidence 0.15 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.09
Although calcineurin was not significantly involved in the Ca2+ threshold for RP induction, it is critical for the GABABR-mediated suppression of RP induction (Kawaguchi and Hirano, 2002).
Positive_regulation (induction) of GABABR
12) Confidence 0.13 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.03
M, Tocris Cookson) to inhibit glutamatergic EPSCs, action potentials, and GABABR activation, respectively.
Positive_regulation (activation) of GABABR associated with action potential
13) Confidence 0.13 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.15
On the other hand, the suppression of sustained CaMKII activation largely depended on the duration of GABABR activation.
Positive_regulation (activation) of GABABR
14) Confidence 0.13 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0.41 Pain Relevance 0.16

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