INT139295

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Context Info
Confidence 0.42
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 11
Disease Relevance 2.93
Pain Relevance 2.43

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

chromosome (Obfc1) nucleus (Obfc1) DNA binding (Obfc1)
Anatomy Link Frequency
neurons 3
spinal trigeminal nucleus 2
spikes 1
SNr 1
STN 1
Obfc1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
substance P 17 99.98 Very High Very High Very High
dopamine receptor 35 99.84 Very High Very High Very High
IPN 4 98.38 Very High Very High Very High
opioid receptor 3 95.80 Very High Very High Very High
Hyperalgesia 2 93.76 High High
Pain 4 93.08 High High
medulla 9 86.64 High High
Raphe 2 85.44 High High
Central nervous system 2 83.04 Quite High
Substantia nigra 24 81.20 Quite High
Disease Link Frequency Relevance Heat
Attention Deficit Hyperactivity Disorder 24 99.64 Very High Very High Very High
Inflammatory Pain 4 98.38 Very High Very High Very High
Dyskinesias 43 97.68 Very High Very High Very High
Catalepsy 91 97.04 Very High Very High Very High
Nociception 2 96.92 Very High Very High Very High
Hyperalgesia 2 93.76 High High
Pain 4 93.08 High High
Parkinson's Disease 49 89.12 High High
Disease 76 74.32 Quite High
Generalized Anxiety Disorder 4 24.56 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The reversal of STN and SNr hyperactivity of 6-OHDA-treated rats by additional PPN lesion suggests an important modulatory influence of the PPN on STN activity.
Gene_expression (reversal) of STN in SNr associated with attention deficit hyperactivity disorder
1) Confidence 0.42 Published 2006 Journal Eur. J. Neurosci. Section Abstract Doc Link 17042796 Disease Relevance 0.46 Pain Relevance 0.18
The reversal of STN and SNr hyperactivity of 6-OHDA-treated rats by additional PPN lesion suggests an important modulatory influence of the PPN on STN activity.
Gene_expression (reversal) of STN in STN associated with attention deficit hyperactivity disorder
2) Confidence 0.14 Published 2006 Journal Eur. J. Neurosci. Section Abstract Doc Link 17042796 Disease Relevance 0.46 Pain Relevance 0.18
It is revealed that 2h after 2.5% formalin injection SP-expression in the dCSF-CNs and STN is upregulated significantly, which may be considered an important role for nociceptive processing.
Gene_expression (expression) of STN in STN associated with nociception and substance p
3) Confidence 0.08 Published 2009 Journal Brain Res. Bull. Section Abstract Doc Link 19103267 Disease Relevance 0.51 Pain Relevance 0.74
To explore whether the dCSF-CNs modulated the orofacial inflammatory pain in rats, we examined behavioral changes with the orofacial formalin test and SP-expression in the dCSF-CNs and spinal trigeminal nucleus (STN) with dual immunohistochemical labeling for light microscopy or immunoelectron microscopy.
Gene_expression (expression) of STN in spinal trigeminal nucleus associated with ipn and substance p
4) Confidence 0.07 Published 2009 Journal Brain Res. Bull. Section Abstract Doc Link 19103267 Disease Relevance 0.45 Pain Relevance 0.80
In these animals, the spontaneous firing rate of STN neurons ranged from 10.3 to 38.9 spikes/sec with a mean of 19.8±4.1 spikes/sec (n?
Gene_expression (neurons) of STN in spikes
5) Confidence 0.06 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704377 Disease Relevance 0.25 Pain Relevance 0
From these results, and in accordance with the glutamatergic nature of STN-SNr transmission responsible for the tonic discharge of SNr neurons (for review, [38]), we can postulate that the decrease in the firing rate of STN neurons could result in a deactivation of SNr neurons with a propagation of irregular discharge patterns.
Gene_expression (transmission) of STN in neurons
6) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704377 Disease Relevance 0.05 Pain Relevance 0
As for the SNr, similar changes were recorded in the STN. ?
Gene_expression (recorded) of STN
7) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704377 Disease Relevance 0 Pain Relevance 0
From these results, and in accordance with the glutamatergic nature of STN-SNr transmission responsible for the tonic discharge of SNr neurons (for review, [38]), we can postulate that the decrease in the firing rate of STN neurons could result in a deactivation of SNr neurons with a propagation of irregular discharge patterns.
Gene_expression (neurons) of STN in neurons
8) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704377 Disease Relevance 0 Pain Relevance 0.06
Responses of STN neurons to ?
Gene_expression (neurons) of STN in neurons
9) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704377 Disease Relevance 0 Pain Relevance 0
The available data on dopamine receptor mRNA is contradictory, but suggest that a portion of the dopamine receptors in the STN are postsynaptically expressed.
Gene_expression (expressed) of STN associated with dopamine receptor
10) Confidence 0.02 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0 Pain Relevance 0.19
Such decrease also correlated with an enhanced expression of PPE-B mRNA, but not that of PPE-A, in both the striatum and the STN, known to also express peptide precursors (Merchenthaler et al., 1997).
Gene_expression (expression) of STN in striatum
11) Confidence 0.01 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2947938 Disease Relevance 0.74 Pain Relevance 0.27

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