INT142172

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Context Info
Confidence 0.02
First Reported 2007
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 5
Disease Relevance 2.62
Pain Relevance 1.62

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

cytosol (Calb1) nucleus (Calb1) intracellular (Calb1)
cytoplasm (Calb1)
Anatomy Link Frequency
globus pallidus 1
inhibitory interneurons 1
Calb1 (Mus musculus)
Calb1 - D28K (2)
Pain Link Frequency Relevance Heat
GABAergic 2 100.00 Very High Very High Very High
cerebral cortex 5 99.36 Very High Very High Very High
depression 76 97.44 Very High Very High Very High
Neuropeptide 4 96.92 Very High Very High Very High
Neurotransmitter 3 96.32 Very High Very High Very High
medulla 5 94.44 High High
excitatory amino acid 1 90.24 High High
Enkephalin 2 87.52 High High
substance P 2 87.24 High High
Glutamate 6 86.48 High High
Disease Link Frequency Relevance Heat
Kernicterus 14 98.88 Very High Very High Very High
Depression 76 97.44 Very High Very High Very High
Dentatorubro-pallidoluysian Atrophy 6 93.68 High High
Neurodegenerative Disease 2 75.00 Quite High
Frailty 2 75.00 Quite High
Sprains And Strains 6 70.40 Quite High
Newborn Jaundice 1 63.64 Quite High
Schizophrenia 14 5.00 Very Low Very Low Very Low
Body Weight 4 5.00 Very Low Very Low Very Low
Disease 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A decrease in the number of parvalbumin-immunoreactive interneurons in the external segment of the globus pallidus was observed predominantly in cases of acute BE, whereas the number of interneurons immunoreactive for calbindin-D28K was reduced in the putamen in cases of chronic postkernicteric BE.
Negative_regulation (reduced) of calbindin-D28K (D28K) in globus pallidus associated with kernicterus
1) Confidence 0.02 Published 2008 Journal Brain Dev. Section Abstract Doc Link 17937977 Disease Relevance 1.23 Pain Relevance 0.19
Thus, our data reinforces the idea that the eCB-system is a critical component of PFC physiology and that deregulation of eCB-mediated synaptic plasticity may participate to the etiology of PFC-related pathologies.


Negative_regulation (deregulation) of eCB
2) Confidence 0.01 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1933592 Disease Relevance 0.22 Pain Relevance 0.12
Finally, in slices pretreated with AM404 (20 µM), an inhibitor of eCB uptake, the “5 min at 10 Hz” protocol was sufficient to induce LTD showing that eCB uptake is an important limiting step in the induction of 2-AG-mediated plasticity (Fig 8).


Negative_regulation (inhibitor) of eCB associated with depression
3) Confidence 0.01 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1933592 Disease Relevance 0.63 Pain Relevance 0.41
The number of interneurons immunoreactive for calbindin-D28K and parvalbumin, markers of GABAergic inhibitory interneurons, were reduced throughout the cerebral cortex, but there was no significant difference in the density of immunoreactive neurons between DRPLA patients of each type.
Negative_regulation (reduced) of calbindin-D28K (D28K) in inhibitory interneurons associated with gabaergic and cerebral cortex
4) Confidence 0.01 Published 2007 Journal Brain Dev. Section Abstract Doc Link 17307319 Disease Relevance 0.55 Pain Relevance 0.90
A small eCB-iLTD (10% eIPSP reduction) persisted in conotoxin. eCB-iLTD was blocked by a microOR agonist in 6/13 slices.
Negative_regulation (blocked) of eCB
5) Confidence 0.00 Published 2008 Journal Psychopharmacology (Berl.) Section Body Doc Link 18097653 Disease Relevance 0 Pain Relevance 0

General Comments

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