INT13572

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Context Info
Confidence 0.36
First Reported 1991
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 31
Total Number 32
Disease Relevance 5.85
Pain Relevance 13.41

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

cell differentiation (Helt) nucleus (Helt) DNA binding (Helt)
Anatomy Link Frequency
neurons 13
GABAergic neurons 5
interneurons 3
dorsal 1
stellate cell 1
Helt (Mus musculus)
Pain Link Frequency Relevance Heat
GABAergic 639 100.00 Very High Very High Very High
amygdala 116 100.00 Very High Very High Very High
medulla 69 100.00 Very High Very High Very High
Neurotransmitter 40 100.00 Very High Very High Very High
gABA 230 99.98 Very High Very High Very High
Glutamate 50 99.98 Very High Very High Very High
Anterior cingulate cortex 129 99.84 Very High Very High Very High
opiate 6 99.32 Very High Very High Very High
Somatosensory cortex 42 98.72 Very High Very High Very High
Locus ceruleus 108 98.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Sleep Disorders 194 99.42 Very High Very High Very High
Generalized Anxiety Disorder 354 98.40 Very High Very High Very High
Targeted Disruption 94 98.00 Very High Very High Very High
Shock 3 93.40 High High
Ganglion Cysts 1 90.88 High High
Increased Venous Pressure Under Development 6 90.16 High High
Urological Neuroanatomy 109 89.84 High High
Primary Sclerosing Cholangitis 171 89.12 High High
Epilepsy 3 83.92 Quite High
Vibrio Infection 15 81.88 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Reelin is an extracellular matrix protein, secreted by GABAergic interneurons, that provides a signal for neural plasticity.
Localization (secreted) of GABAergic in neural associated with gabaergic
1) Confidence 0.36 Published 2007 Journal Brain Res. Section Abstract Doc Link 17174287 Disease Relevance 0.35 Pain Relevance 0.33
Previously, we found that both ethanol and corticotropin releasing factor (CRF) increase GABAergic transmission in mouse and rat CeA neurons, in part by enhancing the release of GABA via activation of presynaptic CRF1 receptors.
Localization (transmission) of neurons in neurons associated with gaba, gabaergic and amygdala
2) Confidence 0.04 Published 2011 Journal Frontiers in Neuroscience Section Abstract Doc Link PMC3024005 Disease Relevance 0 Pain Relevance 0.52
Previously, we found that both ethanol and corticotropin releasing factor (CRF) increase GABAergic transmission in mouse and rat CeA neurons, in part by enhancing the release of GABA via activation of presynaptic CRF1 receptors.
Localization (transmission) of GABAergic in neurons associated with gaba, gabaergic and amygdala
3) Confidence 0.04 Published 2011 Journal Frontiers in Neuroscience Section Abstract Doc Link PMC3024005 Disease Relevance 0 Pain Relevance 0.52
In particular, CB1 protein and mRNA are present at very high levels in cortical GABAergic interneurons (those that release ?
Localization (release) of GABAergic in interneurons associated with gabaergic
4) Confidence 0.03 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2001214 Disease Relevance 0.16 Pain Relevance 0.72
The deficit in vigilance seen in HDC-KO mice might be due, at least in part, to the action of GABA released from ex-HA neurons, the inhibitory action of which is opposed to the normal excitatory actions of histamine release.
Localization (released) of neurons in neurons associated with gaba
5) Confidence 0.02 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2972729 Disease Relevance 0.15 Pain Relevance 0.39
It is thus conceivable that the absence of CHL1 in stellate cell axons may impair GABAergic vesicle endocytosis and GAD65 synaptic localization.
Localization (localization) of GABAergic in stellate cell associated with gabaergic
6) Confidence 0.02 Published 2008 Journal PLoS Biology Section Body Doc Link PMC2689695 Disease Relevance 0.06 Pain Relevance 0.13
Both GABAergic and glycinergic release were enhanced by GluR5 activation in SG neurons
Localization (release) of GABAergic in neurons associated with substantia gelatinosa and gabaergic
7) Confidence 0.02 Published 2006 Journal Mol Pain Section Body Doc Link PMC1570342 Disease Relevance 0 Pain Relevance 0.67
These results indicate that ruthenium red has a dual action on GABA release from GABAergic interneurons: it reduces the amplitude of spontaneous events and increases the frequency of miniature currents.
Localization (release) of GABAergic in interneurons associated with gaba and gabaergic
8) Confidence 0.02 Published 1998 Journal J. Neurophysiol. Section Abstract Doc Link 9819245 Disease Relevance 0 Pain Relevance 0.42
We recorded from postsynaptic neurons distributed across L2–6 (i.e., all the cortical layers that contain excitatory neurons) and, for each one, stimulated presynaptic neurons also distributed across L2–6.
Localization (distributed) of neurons in neurons
9) Confidence 0.02 Published 2011 Journal PLoS Biology Section Body Doc Link PMC3014926 Disease Relevance 0 Pain Relevance 0.34
It is still not known how HCRT regulates REM sleep or muscle tone since HCRT neurons are localized only in the lateral hypothalamus while REM sleep and muscle atonia are generated from the brainstem.
Localization (localized) of neurons in neurons associated with medulla
10) Confidence 0.01 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2709920 Disease Relevance 0.51 Pain Relevance 0.09
To confirm in mice, we examined another region such as the locus coeruleus where the hypocretin-1 receptor is present [26], [27], and did not find hypocretin-2 receptor immunoreactive neurons.
Localization (find) of neurons in neurons associated with locus ceruleus
11) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2709920 Disease Relevance 0.23 Pain Relevance 0.13
A second site is the ventral lateral periaquaductal gray (vlPAG) area where it is also hypothesized that neurons inhibitory to REM sleep are localized [13].
Localization (localized) of neurons in lateral
12) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2709920 Disease Relevance 0.53 Pain Relevance 0.07
The presynaptic glutamate release to the activated neurons is increased and pharmacological inhibition of neuronal activities in the ACC reduced the interest of male mice to female mice.
Localization (release) of neurons in neuronal associated with glutamate and anterior cingulate cortex
13) Confidence 0.01 Published 2009 Journal Mol Brain Section Abstract Doc Link PMC2685783 Disease Relevance 0.09 Pain Relevance 0.52
By using transgenic fosGFP mice, we found that sexual attraction induced functional increases of presynaptic glutamate release to activated neurons in ACC slices.
Localization (release) of neurons in neurons associated with targeted disruption, glutamate and anterior cingulate cortex
14) Confidence 0.01 Published 2009 Journal Mol Brain Section Body Doc Link PMC2685783 Disease Relevance 0.18 Pain Relevance 0.74
For example, the analysis of neurons and neuroendocrine cells of SNAP-25 null mutant mice, generated by homologous recombination-mediated disruption of this t-SNARE gene [3], has demonstrated the selective abrogation of evoked neurotransmission, leaving constitutive release of neurotransmitter in catecholaminergic [4], GABAergic [5], glutamatergic and cholinergic systems [3] intact, despite varying effects on the amplitude and frequency of these transmitter-specific release events.
Localization (release) of GABAergic in neurons associated with neurotransmitter and gabaergic
15) Confidence 0.01 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2600647 Disease Relevance 0 Pain Relevance 0.32
Complex eIPSC are the result of activation and release from several GABAergic and glycinergic axon terminals and thus complex GABAAR and GlyR mediated eIPSCs should not be misinterpreted as evidence of co-release of the two neurotransmitters from the same terminal.
Localization (release) of GABAergic associated with neurotransmitter and gabaergic
16) Confidence 0.01 Published 2009 Journal Mol Pain Section Body Doc Link PMC2689203 Disease Relevance 0 Pain Relevance 0.23
The GABAergic release could be modified by GABAA and GABAB targeted drugs.
Localization (release) of GABAergic associated with gabaergic
17) Confidence 0.01 Published 1993 Journal Neurochem. Res. Section Abstract Doc Link 8097290 Disease Relevance 0 Pain Relevance 0.59
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 GABAergic in GABAergic neurons associated with gabaergic
18) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.18 Pain Relevance 0.54
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 GABAergic in GABAergic neurons associated with gabaergic
19) Confidence 0.01 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 GABAergic in neurons associated with locus ceruleus and gabaergic
20) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2629845 Disease Relevance 0.25 Pain Relevance 0.45

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