INT193832

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Context Info
Confidence 0.13
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 19
Total Number 20
Disease Relevance 6.96
Pain Relevance 8.04

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

Anatomy Link Frequency
neurons 7
GABAergic neurons 7
dorsal 1
Monocyte 1
SLD 1
Ps (Mus musculus)
Pain Link Frequency Relevance Heat
GABAergic 752 100.00 Very High Very High Very High
medulla 114 100.00 Very High Very High Very High
Glutamate 18 98.80 Very High Very High Very High
Inflammation 86 98.72 Very High Very High Very High
Central grey 128 98.36 Very High Very High Very High
monoamine 32 97.76 Very High Very High Very High
Locus ceruleus 128 97.72 Very High Very High Very High
antagonist 32 96.80 Very High Very High Very High
Raphe 48 91.68 High High
Inflammatory response 28 90.80 High High
Disease Link Frequency Relevance Heat
Disease 288 99.98 Very High Very High Very High
Sleep Disorders 128 99.54 Very High Very High Very High
Generalized Anxiety Disorder 608 99.18 Very High Very High Very High
INFLAMMATION 122 98.72 Very High Very High Very High
Urological Neuroanatomy 196 98.36 Very High Very High Very High
Vibrio Infection 16 98.08 Very High Very High Very High
Apoptosis 14 91.32 High High
Frontotemporal Dementia 26 90.52 High High
Alzheimer's Dementia 30 90.20 High High
Brain Disease 8 88.72 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Here, I describe recent findings implicating PS/?
Localization (implicating) of PS
1) Confidence 0.13 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0.74 Pain Relevance 0.30
Monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6) and interleukin-8 (IL-8) are increased by familial AD-linked PS mutations (Sokolova et al., 2009), and mutant PS1 enhances expression of microglial factors that promote differentiation of neural precursor cells into glial fibrillary acidic protein (GFAP)-positive cells (Choi et al., 2008).
Localization (linked) of PS in Monocyte associated with disease
2) Confidence 0.13 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0.66 Pain Relevance 0.20
Determination of PS protein topology is of particular interest because it may facilitate a better understanding of the structural and functional relationship of ?
Localization (topology) of PS
3) Confidence 0.09 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1513131 Disease Relevance 0.98 Pain Relevance 0
PS topology
Localization (topology) of PS
4) Confidence 0.09 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1513131 Disease Relevance 1.00 Pain Relevance 0
These results combined with our previous pharmacological and neuroanatomical results [1], [2], [21] indicate that PS-off GABAergic neurons localized in the vlPAG/dDpMe region inhibit PS onset during W and SWS by means of a tonic inhibitory input to the SLD PS-on neurons.
Localization (localized) of PS-off in neurons associated with gabaergic
5) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.21 Pain Relevance 0.25
From these results, we propose a revised model for PS control in which GABAergic PS-on and PS-off neurons localized in the vlPAG/dDPMe region play leading roles.



Localization (localized) of PS-on in neurons associated with gabaergic
6) Confidence 0.04 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2629845 Disease Relevance 0.07 Pain Relevance 0.47
In contrast, Maloney et al. [3] combining GAD67 and Fos immunohistochemistry proposed that the PS-off GABAergic neurons are localized in the nucleus pontis oralis (PnO).
Localization (localized) of PS-off in GABAergic neurons associated with gabaergic
7) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.43 Pain Relevance 0.48
Based on these previous and the present results, we propose that the PS-on GABAergic neurons localized in the vlPAG inhibit during PS the DRN serotonergic and LC noradrenergic neurons and the co-distributed vlPAG/dDpMe GABAergic PS-off neurons inducing by this way the desinhibition of the SLD PS-on neurons.
Localization (localized) of PS-on in neurons associated with locus ceruleus and gabaergic
8) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.25 Pain Relevance 0.45
Finally, we showed that PS-on neurons triggering PS localized in the SLD are not GABAergic.
Localization (localized) of PS-on in neurons associated with gabaergic
9) Confidence 0.04 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2629845 Disease Relevance 0.08 Pain Relevance 0.48
Altogether, our results indicate that multiple populations of PS-on GABAergic neurons are distributed in the brainstem while only one population of PS-off GABAergic neurons localized in the vlPAG/dDpMe region exist.
Localization (localized) of PS-off in GABAergic neurons associated with medulla and gabaergic
10) Confidence 0.04 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2629845 Disease Relevance 0.07 Pain Relevance 0.47
We recently showed in the rat that neurons generating PS are specifically active during PS (PS-on or REM-on neurons) and localized in the sublaterodorsal tegmental nucleus (SLD).
Localization (localized) of PS-on in neurons
11) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.21 Pain Relevance 0.19
However, since Mus injection in the vlPAG/dDpMe region inhibits at the same time the PS-off and PS-on GABAergic neurons localized in this area and nevertheless induces an increase of PS quantities, it might be concluded that the activation of the vlPAG PS-on GABAergic neurons is not essential to obtain PS.
Localization (localized) of PS-off in GABAergic neurons associated with gabaergic
12) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.07 Pain Relevance 0.55
Combining retrograde tracing with cholera toxin B subunit (CTb) and glutamate decarboxylase (GAD) immunostaining, we proposed that these PS-off GABAergic neurons could be localized in three areas namely the ventrolateral periaqueductal gray (vlPAG) and the dorsal part of the deep mesencephalic reticular nucleus (dDpMe), the caudal pontine reticular nucleus (PnC) and/or the SLD itself [2].
Localization (localized) of PS-off in SLD associated with glutamate, generalized anxiety disorder, gabaergic, vibrio infection and central grey
13) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.42 Pain Relevance 0.33
It might also indicate that the main function of these neurons is to inhibit the co-localized GABAergic PS-off neurons during PS whereas their role in inhibiting the monoaminergic neurons is not essential.
Localization (localized) of PS-off in neurons associated with gabaergic and monoamine
14) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.17 Pain Relevance 0.61
To fill this important gap, we decided to localize all brainstem PS-on or PS-off GABAergic neurons.
Localization (localize) of PS-on in GABAergic neurons associated with medulla and gabaergic
15) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.36 Pain Relevance 0.53
From these results, we propose a revised model for PS control in which GABAergic PS-on and PS-off neurons localized in the vlPAG/dDPMe region play leading roles.



Localization (localized) of PS-off in neurons associated with gabaergic
16) Confidence 0.04 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2629845 Disease Relevance 0.07 Pain Relevance 0.46
To fill this important gap, we decided to localize all brainstem PS-on or PS-off GABAergic neurons.
Localization (localize) of PS-off in GABAergic neurons associated with medulla and gabaergic
17) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.36 Pain Relevance 0.54
Combining CTb and GAD or CTb and Fos immunostaining after PS hypersomnia, we proposed that the PS-on GABAergic neurons at the origin of this inhibition would be localized in the vlPAG and the dorsal paragigantocellular reticular nucleus (DPGi) [6], [7].
Localization (localized) of PS-on in dorsal associated with generalized anxiety disorder, gabaergic and sleep disorders
18) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.57 Pain Relevance 0.63
Our results only partly fit with the recent model of Lu et al. [4] who proposed that the genesis of PS is due to a GABAergic inhibitory reciprocal interaction between PS-on GABAergic neurons localized in the SLD and GABAergic PS-off neurons from the vlPAG/dDpMe region.
Localization (localized) of PS-on in GABAergic neurons associated with gabaergic
19) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.18 Pain Relevance 0.53
However, since Mus injection in the vlPAG/dDpMe region inhibits at the same time the PS-off and PS-on GABAergic neurons localized in this area and nevertheless induces an increase of PS quantities, it might be concluded that the activation of the vlPAG PS-on GABAergic neurons is not essential to obtain PS.
Localization (localized) of PS-on in GABAergic neurons associated with gabaergic
20) Confidence 0.02 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.07 Pain Relevance 0.55

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