INT63383

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.48
First Reported 1996
Last Reported 2010
Negated 3
Speculated 4
Reported most in Body
Documents 77
Total Number 81
Disease Relevance 22.28
Pain Relevance 44.61

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 (Cnr1) aging (Cnr1) plasma membrane (Cnr1)
signal transducer activity (Cnr1)
Anatomy Link Frequency
brain 6
synapses 3
granule cells 2
ventricle 1
spinal nerve 1
Cnr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Cannabinoid 2246 100.00 Very High Very High Very High
agonist 1702 100.00 Very High Very High Very High
mu opioid receptor 547 100.00 Very High Very High Very High
antagonist 293 100.00 Very High Very High Very High
Cannabinoid receptor 257 100.00 Very High Very High Very High
Dopamine 95 100.00 Very High Very High Very High
Sciatic nerve 15 100.00 Very High Very High Very High
Spinal nerve ligature 2 100.00 Very High Very High Very High
tolerance 1048 99.88 Very High Very High Very High
fluoxetine 34 99.76 Very High Very High Very High
Disease Link Frequency Relevance Heat
Urological Neuroanatomy 230 100.00 Very High Very High Very High
Hypersensitivity 26 100.00 Very High Very High Very High
Targeted Disruption 152 99.96 Very High Very High Very High
Neurodegenerative Disease 137 99.04 Very High Very High Very High
Suicidal Behaviour 24 99.00 Very High Very High Very High
Epilepsy 308 98.96 Very High Very High Very High
Neuropathic Pain 270 98.88 Very High Very High Very High
Cancer Pain 5 98.48 Very High Very High Very High
Spasticity 58 98.18 Very High Very High Very High
Bordatella Infection 85 98.08 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The thio analogs of both anandamide and (R)-methanandamide showed very weak affinity for CB1.
CB1 Binding (affinity) of
1) Confidence 0.48 Published 1996 Journal J. Med. Chem. Section Abstract Doc Link 8893848 Disease Relevance 0 Pain Relevance 0.04
The data provides strong evidence that the CB1 receptor-ligand interaction is essential for the antinociceptive effect.
CB1 Binding (interaction) of associated with antinociceptive
2) Confidence 0.48 Published 1996 Journal Neuroreport Section Abstract Doc Link 8730837 Disease Relevance 0.12 Pain Relevance 0.60
In normal animals, CB1R binding can inhibit glutamatergic input arising from mossy cells [48].
CB1R Binding (binding) of
3) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2871782 Disease Relevance 0.35 Pain Relevance 0.47
Many cannabinoid agonists bind both CB1R and CB2R, and AEA is also an agonist at TRPV1 receptors, activation of which can enhance release of neurotransmitter by increasing intracellular concentrations of Ca2+ [63].
CB1R Binding (bind) of associated with neurotransmitter, cannabinoid and agonist
4) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2871782 Disease Relevance 0.34 Pain Relevance 0.26
The loss of hilar mossy cells and GABAergic interneurons during the development of TLE in similar models [55] and the concomitant loss of CB1R associated with these nerve terminals could contribute to a reduction in the density of CB1R observed in immunohistochemical analyses.
CB1R Binding (associated) of in nerve associated with epilepsy and gabaergic
5) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2871782 Disease Relevance 0.58 Pain Relevance 0.37
Although it has been reported that CBD binds with a low affinity to the CB1 receptor, its mode of action on neurogenesis seems to involve the CB1 receptor since CBD had no effect on CB1-/- animals.
CB1 receptor Binding (binds) of associated with neurodegenerative disease
6) Confidence 0.48 Published 2010 Journal Cell Commun Signal Section Body Doc Link PMC2898685 Disease Relevance 0.70 Pain Relevance 0.15
Here we have evaluated the interactions between the CB1 cannabinoid receptors and the endogenous opioid system by assaying a number of well-characterized opioid responses, e.g. antinociception and stress-mediated effects, on mutant mice in which the CB1 receptor gene was invalidated.
CB1 Binding (interactions) of associated with stress, antinociception, cannabinoid receptor, endogenous opioid and opioid
7) Confidence 0.47 Published 2000 Journal Eur. J. Neurosci. Section Abstract Doc Link 10712632 Disease Relevance 0.25 Pain Relevance 1.06
Both purinergic and cannabinoid systems interact with dopamine neurotransmission (through A2A and CB1 receptors, respectively).
CB1 Binding (interact) of associated with dopamine and cannabinoid
8) Confidence 0.47 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15450100 Disease Relevance 0.21 Pain Relevance 0.57
The results presented herein raise the possibility that anandamide may not be producing all of its effects by a direct interaction with the CB1 receptor.
CB1 receptor Binding (interaction) of
9) Confidence 0.44 Published 1998 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9495885 Disease Relevance 0 Pain Relevance 0.27
Therefore, this study was undertaken to determine whether its interaction with the CB1 receptor in brain was identical to that of delta 9-THC.
CB1 receptor Spec (whether) Binding (interaction) of in brain
10) Confidence 0.44 Published 1998 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9495885 Disease Relevance 0.09 Pain Relevance 0.39
Interestingly, TRPV1 binding was increased in the striatum of DAT KO mice, while CB1 receptor binding was unaffected.
CB1 receptor Binding (binding) of in striatum
11) Confidence 0.43 Published 2006 Journal Biol. Psychiatry Section Body Doc Link 16199010 Disease Relevance 0.17 Pain Relevance 0
Another nonpsychoactive endogenous compound, the anti-inflammatory mediator PEA (Lambert and Di Marzo 1999), also induced a significant, albeit transient inhibition of spasticity (Pryce and Baker 2007); however, the mechanism of action of this compound, which does not bind appreciably to CB1 or CB2 receptors, is still a matter of speculation (Lambert and Di Marzo 1999).
CB1 Neg (not) Binding (bind) of associated with spasticity and inflammation
12) Confidence 0.43 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2626929 Disease Relevance 1.29 Pain Relevance 0.42
We evaluated delta-9 tetrahydrocannabinol (Delta9-THC), delta-8 tetrahydrocannabinol (Delta8-THC), CP55,940 (CP55), 1-deoxy-11-hydroxy-Delta8-THC-dimethylheptyl (deoxy-HU210, a CB2-selective cannabinoid that also binds the CB1 receptor) and the endogenous cannabinoid anandamide (ANA) via i.c.v. and/or intrathecal (i.t.) routes of administration, alone and in combination with SR141716A (SR), a CB1 antagonist, using the tail-flick test.
CB1 receptor Binding (binds) of in tail associated with antagonist, cannabinoid, tail-flick and intrathecal
13) Confidence 0.39 Published 1998 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9732392 Disease Relevance 0 Pain Relevance 0.48
Activation of postsynaptic receptors, at diverse neuronal types, induces the release of endogenous cannabinoid compounds that move backwards across the synapse, until reaching the cannabinoid CB1 receptor, to which they bind, therefore inhibiting further neurotransmitter release.
cannabinoid CB1 receptor Binding (bind) of in synapse associated with neurotransmitter and cannabinoid
14) Confidence 0.39 Published 2007 Journal Neural Plasticity Section Body Doc Link PMC1906867 Disease Relevance 0.06 Pain Relevance 0.37
Cannabinoids exert their effect through interactions with specific endogenous CB1 and CB2 cannabinoid receptors [6,7] that are present in mammalian tissues.
CB1 Binding (interactions) of associated with cannabinoid receptor and cannabinoid
15) Confidence 0.38 Published 2010 Journal Behav Brain Funct Section Body Doc Link PMC2858089 Disease Relevance 0.19 Pain Relevance 0.50
For this purpose, partial ligation of the sciatic nerve was performed in CB1 cannabinoid receptor knockout mice and their wild-type littermates.
CB1 cannabinoid receptor Spec (partial) Binding (ligation) of in sciatic nerve associated with targeted disruption, cannabinoid receptor and sciatic nerve
16) Confidence 0.37 Published 2006 Journal Neuropharmacology Section Abstract Doc Link 16169563 Disease Relevance 1.12 Pain Relevance 1.08
This suggests that CB1R could be made in the cell body of the granule cells and be trafficked to the terminals.
CB1R Binding (trafficked) of in granule cells
17) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2871782 Disease Relevance 0.45 Pain Relevance 0.24
Binding CB1R suppressed secondary population afterdischarges subsequent to antidromic activation of the granule cells.
CB1R Binding (Binding) of in granule cells
18) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2871782 Disease Relevance 0.38 Pain Relevance 0.22
WIN55,212-2 desensitized its own analgesic response and, as expected for agonists sharing the receptor, it was also desensitized by other CB1R agonists, such as methanandamide, ACEA, and THC.
CB1R Binding (desensitized) of associated with analgesic and agonist
19) Confidence 0.37 Published 2009 Journal Mol Pain Section Body Doc Link PMC2657119 Disease Relevance 0 Pain Relevance 1.54
Then, in order to directly evaluate the presence of the CB1Rs in the synaptosomal membrane, we developed two antibodies that recognize extracellular domains on the CB1 receptor: one is directed against a peptide sequence in the N terminus (Nt) and the other against the first extracellular loop (1EL).
CB1 receptor Binding (recognize) of
20) Confidence 0.37 Published 2009 Journal Mol Pain Section Body Doc Link PMC2657119 Disease Relevance 0 Pain Relevance 0.44

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox