INT112099

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Context Info
Confidence 0.40
First Reported 2003
Last Reported 2008
Negated 0
Speculated 1
Reported most in Body
Documents 2
Total Number 10
Disease Relevance 6.17
Pain Relevance 8.16

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

plasma membrane (Dlg2) cytoplasm (Dlg2)
Anatomy Link Frequency
cerebellum 3
neurons 1
cortex 1
hippocampus 1
Dlg2 (Mus musculus)
Pain Link Frequency Relevance Heat
Physical dependence 135 99.32 Very High Very High Very High
Dorsal horn 108 98.72 Very High Very High Very High
Acute pain 10 98.52 Very High Very High Very High
tolerance 225 98.36 Very High Very High Very High
Morphine 693 98.28 Very High Very High Very High
Hippocampus 27 98.24 Very High Very High Very High
Analgesic 126 97.92 Very High Very High Very High
Pain 57 97.72 Very High Very High Very High
Central nervous system 99 97.52 Very High Very High Very High
Lasting pain 76 97.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 460 100.00 Very High Very High Very High
Drug Dependence 135 99.32 Very High Very High Very High
Pain 167 98.52 Very High Very High Very High
Nociception 10 97.36 Very High Very High Very High
Pathologic Processes 18 97.08 Very High Very High Very High
Cerebellar Diseases 9 95.24 Very High Very High Very High
Nervous System Injury 10 93.88 High High
Hypersensitivity 27 81.76 Quite High
Substance Withdrawal Syndrome 36 80.56 Quite High
INFLAMMATION 18 39.52 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Targeted disruption of the PSD-93 gene reduces not only surface NR2A and NR2B expression but also NMDAR-mediated excitatory postsynaptic currents and potentials, without affecting surface AMPA receptor expression or its synaptic function, in the regions mentioned above.
Negative_regulation (disruption) of PSD-93 gene associated with targeted disruption
1) Confidence 0.40 Published 2003 Journal J. Neurosci. Section Abstract Doc Link 12890763 Disease Relevance 0.47 Pain Relevance 0.55
The present study showed that PSD-93 deficiency significantly inhibited acute and chronic morphine analgesic tolerance, enhancing formalin-induced pain behaviors, and withdrawal-induced jumping following repeated morphine injection.
Negative_regulation (deficiency) of PSD-93 associated with pain, analgesic, tolerance, withdrawal and morphine
2) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.96 Pain Relevance 1.54
Our previous study showed that targeted disruption of PSD-93 gene significantly attenuates the NMDA-stimulated increase in cyclic guanosine 3', 5'-monophosphate in the cultured forebrain cortex neurons [30].
Negative_regulation (disruption) of PSD-93 gene in neurons associated with targeted disruption
3) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.97 Pain Relevance 1.16
However, PSD-93 deficiency did not markedly change the amounts of NR2A and NR2B in either synaptosomal or total soluble fractions from cerebellum.
Negative_regulation (deficiency) of PSD-93 in cerebellum
4) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.29 Pain Relevance 0.40
It is very likely that PSD-95 and SAP102 compensate for the deficiency of PSD-93 to anchor and target NMDARs at synapses in hippocampus and cerebellum neurons of PSD-93 KO mice.
Negative_regulation (deficiency) of PSD-93 in hippocampus associated with targeted disruption and hippocampus
5) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.33 Pain Relevance 0.56
Our quantitative Western blot analysis showed that PSD-93 deficiency significantly reduced the levels of NR2A and NR2B proteins in the synaptosomal membrane fractions of dorsal horn and forebrain cortex but did not affect their expression in the total soluble fractions of these two regions.
Negative_regulation (deficiency) of PSD-93 in cortex associated with dorsal horn
6) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.40 Pain Relevance 0.63
An important observation in the present study is that PSD-93 deficiency produces distinct effects on synaptic NMDAR expression in different regions of the CNS.
Negative_regulation (deficiency) of PSD-93 associated with central nervous system
7) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.47 Pain Relevance 0.76
Thus, targeted disruption of PSD-93 or perturbing NMDAR-PSD-93 interaction might be a better strategy for prevention and/or treatment of persistent pain and opioid tolerance and physical dependence in clinic.
Negative_regulation (disruption) of PSD-93 associated with pain, targeted disruption, physical dependence, lasting pain, tolerance and opioid
8) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 1.22 Pain Relevance 1.48
In the present study, we examined whether PSD-93 deficiency affected synaptic NR2A and NR2B expression in two major pain-related regions [18,19], spinal cord and forebrain cortex, and a motor and coordination-related region [20], cerebellum, of the CNS.
Spec (whether) Negative_regulation (deficiency) of PSD-93 in cerebellum associated with pain, central nervous system and spinal cord
9) Confidence 0.38 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.74 Pain Relevance 0.52
It is very likely that PSD-95 and SAP102 compensate for the deficiency of PSD-93 to anchor and target NMDARs at synapses in hippocampus and cerebellum neurons of PSD-93 KO mice.
Negative_regulation (deficiency) of PSD-93 in cerebellum associated with targeted disruption and hippocampus
10) Confidence 0.13 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0.33 Pain Relevance 0.56

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