INT88587

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Context Info
Confidence 0.46
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 10
Total Number 10
Disease Relevance 3.00
Pain Relevance 7.35

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

transport (Chrna6) plasma membrane (Chrna6)
Anatomy Link Frequency
dorsal horn 2
dopaminergic neurons 2
cholinergic neurons 1
inner ear 1
interneurons 1
Chrna6 (Mus musculus)
Pain Link Frequency Relevance Heat
spinal dorsal horn 28 99.96 Very High Very High Very High
Pain 43 99.82 Very High Very High Very High
Nicotine 130 99.64 Very High Very High Very High
intrathecal 19 99.56 Very High Very High Very High
gABA 34 99.40 Very High Very High Very High
agonist 25 99.00 Very High Very High Very High
Analgesic 33 98.38 Very High Very High Very High
antagonist 21 97.76 Very High Very High Very High
Cannabinoid receptor 1 97.36 Very High Very High Very High
GABA receptor 15 97.28 Very High Very High Very High
Disease Link Frequency Relevance Heat
Low Back Pain 21 99.82 Very High Very High Very High
Targeted Disruption 23 97.44 Very High Very High Very High
Pain 24 96.00 Very High Very High Very High
Nociception 60 94.68 High High
Neuropathic Pain 27 84.60 Quite High
Drug Dependence 9 81.08 Quite High
Cannabis Dependence 9 77.32 Quite High
Nicotine Addiction 19 72.04 Quite High
Ganglion Cysts 97 70.28 Quite High
Hyperalgesia 8 50.40 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the spinal dorsal horn, activation of the nicotinic acetylcholine receptors (nAChR) by exogenously applied agonists is known to enhance inhibitory synaptic transmission, and to produce analgesia.
Positive_regulation (activation) of nAChR in dorsal horn associated with spinal dorsal horn, agonist and analgesia
1) Confidence 0.46 Published 2006 Journal Pain Section Abstract Doc Link 16781069 Disease Relevance 0.21 Pain Relevance 0.45
Since the first targeted disruption in 1995 of the gene encoding the beta2-subunit of the nicotinic acetylcholine receptor (nAChR), all but a few of the mammalian nAChR subunits have been disrupted (i.e. alpha7, alpha4, alpha3, alpha9, beta4 and beta3).
Positive_regulation (disrupted) of nAChR associated with targeted disruption
2) Confidence 0.39 Published 2000 Journal Trends Pharmacol. Sci. Section Abstract Doc Link 10838608 Disease Relevance 0.26 Pain Relevance 0.12
These results demonstrate that in nigral dopaminergic neurons, nicotine can elicit Ca2+ mobilization via activation of two distinct nAChR subtypes: that of beta2-subunit-containing nAChR followed by activation of Na+ channel and T-type Ca2+ channels, and/or activation of alpha7-subunit-containing nAChR.
Positive_regulation (activation) of nAChR in dopaminergic neurons associated with nicotine
3) Confidence 0.33 Published 2000 Journal Eur. J. Neurosci. Section Abstract Doc Link 10947823 Disease Relevance 0 Pain Relevance 0.69
The Ca2+ influx due to nAChR activation is subsequently amplified by the recruitment of intracellular Ca2+ stores.
Positive_regulation (activation) of nAChR
4) Confidence 0.22 Published 2000 Journal Eur. J. Neurosci. Section Abstract Doc Link 10947823 Disease Relevance 0 Pain Relevance 0.56
These results demonstrate that in nigral dopaminergic neurons, nicotine can elicit Ca2+ mobilization via activation of two distinct nAChR subtypes: that of beta2-subunit-containing nAChR followed by activation of Na+ channel and T-type Ca2+ channels, and/or activation of alpha7-subunit-containing nAChR.
Positive_regulation (activation) of nAChR in dopaminergic neurons associated with nicotine
5) Confidence 0.19 Published 2000 Journal Eur. J. Neurosci. Section Abstract Doc Link 10947823 Disease Relevance 0 Pain Relevance 0.61
Using microarray analyses, we have defined global gene expression alterations with respect to the wild type condition brought about as a consequence of ablation of the key nicotinic subunit responsible for nAChR activity in the inner ear.
Positive_regulation (responsible) of nAChR in inner ear
6) Confidence 0.09 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2816210 Disease Relevance 0 Pain Relevance 0
The presence of tonic nAChR activation of inhibitory GABA interneurons is supported by many reports that nAChR agonists enhance inhibitory postsynaptic currents (IPSCs), possibly through GABAergic or glycinergic activities in the dorsal horn of the spinal cord [12-15,33].
Positive_regulation (activation) of nAChR in dorsal horn associated with gaba, gabaergic, dorsal horn, agonist and spinal cord
7) Confidence 0.07 Published 2007 Journal Mol Pain Section Body Doc Link PMC2234393 Disease Relevance 0.65 Pain Relevance 1.50
These findings suggest that primary afferent cholinergic neurons produce tonic inhibition of spinal pain through nAChR activation, and that intrathecal administration of nicotine rescues the loss of tonic cholinergic inhibition.



Positive_regulation (activation) of nAChR in cholinergic neurons associated with low back pain, pain, nicotine and intrathecal
8) Confidence 0.07 Published 2007 Journal Mol Pain Section Abstract Doc Link PMC2234393 Disease Relevance 0.73 Pain Relevance 0.85
Thus, the nicotine-induced analgesic effects in AS-ODN treated mice are likely to be attributed to the loss of tonic nAChR activation of inhibitory GABA interneurons.
Positive_regulation (activation) of nAChR in interneurons associated with gaba, analgesic and nicotine
9) Confidence 0.07 Published 2007 Journal Mol Pain Section Body Doc Link PMC2234393 Disease Relevance 0.53 Pain Relevance 1.42
Specifically, nicotine operates through activation of nicotinic acetylcholine receptor (nAChR) complexes; delta9-THC operates through activation of the neural cannabinoid receptor, CB1R.
Positive_regulation (activation) of nAChR in neural associated with cannabinoid receptor and nicotine
10) Confidence 0.02 Published 2007 Journal BMC Genet Section Body Doc Link PMC1978498 Disease Relevance 0.63 Pain Relevance 1.14

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