INT56239

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Context Info
Confidence 0.26
First Reported 1993
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 20
Total Number 29
Disease Relevance 14.05
Pain Relevance 18.80

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

nuclear envelope (Rtn4) aging (Rtn4) endoplasmic reticulum (Rtn4)
plasma membrane (Rtn4) protein complex (Rtn4) cytoplasm (Rtn4)
Anatomy Link Frequency
neurons 7
DRG 3
neural 2
spike 1
nociceptors 1
Rtn4 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
addiction 74 99.98 Very High Very High Very High
sodium channel 211 99.96 Very High Very High Very High
nav1.8 134 99.68 Very High Very High Very High
Sciatic nerve 94 99.68 Very High Very High Very High
withdrawal 62 99.62 Very High Very High Very High
dorsal root ganglion 753 99.60 Very High Very High Very High
Eae 790 99.52 Very High Very High Very High
antagonist 3 98.96 Very High Very High Very High
hyperexcitability 203 98.52 Very High Very High Very High
Paresthesia 1 98.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Ganglion Cysts 811 99.60 Very High Very High Very High
Injury 903 99.52 Very High Very High Very High
Dysesthesia 1 98.44 Very High Very High Very High
Pain 61 98.20 Very High Very High Very High
Neuropathic Pain 142 97.56 Very High Very High Very High
Targeted Disruption 30 95.72 Very High Very High Very High
Hyperalgesia 114 92.56 High High
Nervous System Injury 180 91.72 High High
Nociception 56 87.76 High High
Aging 2 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It is concluded that TTXS currents in DRG are, like TTX-R currents, enhanced by cAMP but whilst the pharmacology of TTXR channels with respect to lidocaine is altered, that to TTXS channels is not.
Positive_regulation (enhanced) of TTX-R in DRG associated with lidocaine
1) Confidence 0.26 Published 2006 Journal Neuropharmacology Section Abstract Doc Link 16930635 Disease Relevance 0.07 Pain Relevance 0.61
The sodium conductance-voltage curve also was shifted by tetramethrin in the hyperpolarizing direction in both TTX-S and TTX-R channels, and the latter was affected more strongly than the former.
Positive_regulation (direction) of TTX-R
2) Confidence 0.23 Published 1994 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 8071852 Disease Relevance 0.12 Pain Relevance 0.66
Cell-attached patch recordings showed that the slope conductance of single TTX-S and TTX-R channels was 14.6 pS and 7.8 pS, respectively.
Positive_regulation (conductance) of TTX-R
3) Confidence 0.10 Published 2002 Journal J. Med. Dent. Sci. Section Abstract Doc Link 12160226 Disease Relevance 0.16 Pain Relevance 0.46
Riluzole shifted the voltage dependence of activation of TTX-R sodium channels in the depolarizing direction more than that of TTX-S sodium channels.
Positive_regulation (activation) of TTX-R associated with addiction and sodium channel
4) Confidence 0.08 Published 1997 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9262334 Disease Relevance 0.08 Pain Relevance 0.83
Voltage dependence of activation of TTX-R and TTX-S Na+ currents in small-slow and small-fast neurons is not altered by CCD and CCI
Positive_regulation (activation) of TTX-R in neurons associated with addiction and eae
5) Confidence 0.08 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 0.81 Pain Relevance 0.42
In both small slow and fast neurons, neither CCD nor CCI treatment significantly altered parameters of activation of the TTX-R and TTX-S Na+ currents such as V1/2, k, activation threshold, and voltage range of the maximum inward current fell in.
Positive_regulation (activation) of TTX-R in neurons associated with eae
6) Confidence 0.08 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 0.36 Pain Relevance 0.26
Recent studies have shown that CCD causes a decrease in fast-inactivating K+ current [15] and an increase in expression of a hyperpolarization-activated cation current (Ih), in addition to an increase in TTX-R Na+ currents in cutaneous, medium-sized DRG neurons [55].
Positive_regulation (increase) of TTX-R in neurons associated with dorsal root ganglion
7) Confidence 0.08 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 0.85 Pain Relevance 0.69
The results showed both of a decrease in mechanical withdrawal thresholds and an increase of TTX-R sodium channel current density in DRG neurons in group B were significantly lower than those of group A at 24 h and 48 h after the operation (P<0.05).
Positive_regulation (increase) of TTX-R in DRG associated with sodium channel and withdrawal
8) Confidence 0.07 Published 2008 Journal Brain Res. Section Abstract Doc Link 18400213 Disease Relevance 0.23 Pain Relevance 0.73
NEM caused a change in the voltage-dependence of the activation of TTX-R sodium channel unlike TTX-S sodium channel.
Positive_regulation (activation) of TTX-R associated with addiction and sodium channel
9) Confidence 0.06 Published 2000 Journal Brain Res. Section Abstract Doc Link 10677599 Disease Relevance 0.15 Pain Relevance 0.81
Effects of CCD and CCI on the voltage dependence activation of TTX-R and TTX-S currents were examined and analyzed.
Positive_regulation (activation) of TTX-R associated with addiction and eae
10) Confidence 0.06 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 0.32 Pain Relevance 0.24
In addition, our results show that inactivation of the TTX-R and TTX-S currents are slowed down by CCD and/or CCI in the small-fast neurons.
Positive_regulation (inactivation) of TTX-R in neurons associated with eae
11) Confidence 0.06 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 0.41 Pain Relevance 0.59
These findings might support a possibility that either upregulation or downregulation of the TTX-R or TTX-S current densities in the injured medium-sized [15,8] and small DRG neurons, which express both Nav1.8 and Nav1.7 channels, can produce neural hyperexcitability.
Positive_regulation (upregulation) of TTX-R in neural associated with dorsal root ganglion, nav1.8, hyperexcitability and nav1.7
12) Confidence 0.06 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 0.71 Pain Relevance 1.01
A recent study indicates that the cutaneous, medium-sized dissociated CCD DRG neurons exhibit an increase in TTX-R Na+ currents [15].
Positive_regulation (increase) of TTX-R in neurons associated with dorsal root ganglion
13) Confidence 0.06 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 1.53 Pain Relevance 1.47
A recent study shows that TTX-R Na+ currents are upregulated in the cutaneous medium-sized CCD DRG neurons [15], which is somewhat different from the findings in axon injury models.
Positive_regulation (upregulated) of TTX-R in neurons associated with dorsal root ganglion and injury
14) Confidence 0.05 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 2.31 Pain Relevance 1.86
The differential effects in the TTX-R and TTX-S Na+ current induced by CCD and CCI may contribute partly to certain differences in neural excitability and behavioral manifestations between the two models [13].
Positive_regulation (induced) of TTX-R in neural associated with eae
15) Confidence 0.05 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 1.04 Pain Relevance 1.22
TTX-R Na+ channel is also found upregulated in the sciatic nerve axons at the site of injury [32] and redistributed in the uninjured adjacent axons of DRG neurons [33].
Positive_regulation (upregulated) of TTX-R in neurons associated with dorsal root ganglion, injury and sciatic nerve
16) Confidence 0.05 Published 2008 Journal Mol Pain Section Body Doc Link PMC2427019 Disease Relevance 1.48 Pain Relevance 1.15
Previous exposure of cells to the endothelin-A (ET(A)) receptor antagonist BQ-123 (1 microm) prevented ET-1-induced shifts in TTX-R activation.
Positive_regulation (activation) of TTX-R associated with antagonist
17) Confidence 0.03 Published 2002 Journal J. Neurosci. Section Abstract Doc Link 12151509 Disease Relevance 0.42 Pain Relevance 0.83
These results demonstrate that the algogenic peptide ET-1 induces ET(A) receptor-mediated, hyperpolarizing shifts in the voltage-dependent activation of TTX-R Na+ channels, a potential mechanism for selective excitation by ET-1 of nociceptors that we observed in vivo.
Positive_regulation (activation) of TTX-R in nociceptors associated with algogenic and nociceptor
18) Confidence 0.03 Published 2002 Journal J. Neurosci. Section Abstract Doc Link 12151509 Disease Relevance 0.33 Pain Relevance 0.66
Previous studies involving neuropathic states have suggested that pain/paresthesia is modulated by a subset of sodium channels, including downregulation and/or upregulation of TTX-R and TTX-S sodium channels, respectively.
Positive_regulation (upregulation) of TTX-R associated with pain, paresthesia, neuropathic pain and sodium channel
19) Confidence 0.03 Published 2010 Journal J. Orthop. Res. Section Abstract Doc Link 19877286 Disease Relevance 0.50 Pain Relevance 1.18
Increases in TTX-R and TTX-S I(Na) thus coincide with axotomy-induced increases in excitability and alterations in spike shape across the whole population of sensory neurons.
Positive_regulation (Increases) of TTX-R in spike
20) Confidence 0.03 Published 2002 Journal J. Neurophysiol. Section Abstract Doc Link 12424291 Disease Relevance 0.16 Pain Relevance 0.12

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