INT223568

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Context Info
Confidence 0.65
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 21
Total Number 21
Disease Relevance 5.83
Pain Relevance 6.12

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 (GYPE)
Anatomy Link Frequency
neurons 4
synapses 2
caudate nucleus 1
striatum 1
globus pallidus 1
GYPE (Homo sapiens)
Pain Link Frequency Relevance Heat
Dopamine 957 100.00 Very High Very High Very High
midbrain 60 100.00 Very High Very High Very High
dopamine receptor 177 99.84 Very High Very High Very High
Enkephalin 28 99.84 Very High Very High Very High
gABA 153 99.64 Very High Very High Very High
GABAergic 193 99.48 Very High Very High Very High
Neuropeptide 19 98.70 Very High Very High Very High
substance P 11 98.42 Very High Very High Very High
cerebral cortex 57 98.02 Very High Very High Very High
Pyramidal cell 81 97.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Disease 537 99.16 Very High Very High Very High
Dyskinesias 67 98.48 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 62 98.18 Very High Very High Very High
Sleep Disorders 234 98.00 Very High Very High Very High
Generalized Anxiety Disorder 22 94.92 High High
Syndrome 165 93.36 High High
Cancer 49 93.28 High High
Bladder Cancer 32 93.00 High High
Cognitive Disorder 32 91.92 High High
Parkinson's Disease 257 87.80 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Next, the same cross- sections used for quantification of LYVE-1 were double labeled with LYVE-1 and an anti-goat polyclonal antibody against Ki-67(M-19), a nuclear protein expressed in proliferating cells that may be required for maintaining cell proliferation [32,33], and that provides the same value for proliferation index as BrdU in urothelial cancer cells [33].
Gene_expression (expressed) of M-19 associated with cancer
1) Confidence 0.65 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2241841 Disease Relevance 0.41 Pain Relevance 0
The STN excites the GPe.
Gene_expression (excites) of GPe
2) Confidence 0.48 Published 2010 Journal Philosophical transactions. Series A, Mathematical, physical, and engineering sciences Section Body Doc Link PMC2944387 Disease Relevance 0.40 Pain Relevance 0.07
S represents the current injected into these cells from the GPe synapses.
Gene_expression (synapses) of GPe in synapses
3) Confidence 0.48 Published 2010 Journal Philosophical transactions. Series A, Mathematical, physical, and engineering sciences Section Body Doc Link PMC2944387 Disease Relevance 0 Pain Relevance 0.07
In addition, GPe lesions do not appear to reduce drug-induced dyskinesias, as predicted by the model (Blanchet et al. 1994).
Gene_expression (lesions) of GPe associated with dyskinesias
4) Confidence 0.16 Published 2010 Journal J Neural Transm Section Body Doc Link PMC3000910 Disease Relevance 0.43 Pain Relevance 0.04
For example, studies have reported decreased levels of dynorphin-like immunoreactivity in the striatum and globus pallidus (Haber et al 1986; Haber and Wolfer 1992), decreased subcortical levels of serotonin (Anderson et al 1992), increased numbers of neurons expressing parvalbumin in the globus pallidus pars internus (GPi) and decreased numbers of neurons expressing parvalbumin in the caudate nucleus and globus pallidus pars externus (GPe) (Kalanithi et al 2005).
Gene_expression (expressing) of GPe in globus pallidus associated with dynorphin and serotonin
5) Confidence 0.12 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2646643 Disease Relevance 0.86 Pain Relevance 0.17
It can therefore be inferred that the loss of D2 postsynaptic and presynaptic inhibition in the striatum and GPe would result in hyperactivity of the striatopallidal neurons, resulting in inhibition (presumably GABA-mediated) of the GPe neurons, which would then result in increased arousal.
Gene_expression (neurons) of GPe in neurons associated with gaba and attention deficit hyperactivity disorder
6) Confidence 0.08 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.24 Pain Relevance 0.34
D1 and D2 dopaminergic receptors are abundantly expressed in the cerebral cortex while D1, D2, D3, and D5 receptors are expressed in the striatum and D2, D3, and D5 receptors are expressed in the GPe.
Gene_expression (expressed) of GPe in striatum associated with cerebral cortex
7) Confidence 0.08 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0 Pain Relevance 0.39
Hence, it can be concluded that the GPe may be one of the many cell groups, including the basal forebrain, thalamus, lateral hypothalamus, LC, and VTA, that directly modulate cortical activity.


Gene_expression (one) of GPe in thalamus associated with thalamus
8) Confidence 0.08 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.32 Pain Relevance 0.53
Most GPe neurons have been shown to fire more slowly and in a bursting pattern following the loss of dopamine inputs, suggesting that the loss of dopamine inputs results in hypoactivity of the GPe neurons.
Gene_expression (neurons) of GPe in neurons associated with dopamine
9) Confidence 0.08 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.06 Pain Relevance 0.35
Thus, these results suggest that GPe neurons target both GABAergic interneurons and glutamatergic pyramidal neurons in the cortex, and that these two regions are reciprocally connected.
Gene_expression (neurons) of GPe in neurons associated with pyramidal cell and gabaergic
10) Confidence 0.08 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.26 Pain Relevance 0.26
In addition to these major neurotransmitters, BG neurons also contain other transmitters or neuropeptides, including enkephalin (ENK) and dynorphin in striatal MSNs; substance P, neuropeptide Y and nitric oxide in the striatal interneurons; and ENK in the GPe neurons.


Gene_expression (neurons) of GPe in GPe associated with neurotransmitter, dynorphin, neuropeptide, enkephalin and substance p
11) Confidence 0.08 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.33 Pain Relevance 0.89
The major source of dopamine in the BG is the midbrain dopaminergic neurons, particularly the SNc (A9 group), and these neurons primarily target the striatum, GPe and GPi.
Gene_expression (source) of GPe in neurons associated with dopamine and midbrain
12) Confidence 0.07 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.71 Pain Relevance 0.52
The GPe, principally sends GABAergic projections to the STN (Albin et al., 1989; Alexander et al., 1990; DeLong, 1990) but anatomical studies have revealed the existence of new efferent projections of the GPe to the two output structures of the basal ganglia (Hazrati et al., 1990; Kincaid et al., 1991).
Gene_expression (projections) of GPe in basal ganglia associated with gabaergic
13) Confidence 0.06 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2947938 Disease Relevance 0 Pain Relevance 0.08
There is also evidence for postsynaptic expression of D2LRs in GPe.
Gene_expression (expression) of GPe
14) Confidence 0.05 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0 Pain Relevance 0.19
Low levels of D2-receptor protein labeling have been detected in human GPe (Levey et al., 1993) and in postsynaptic structures in the rat (Yung et al., 1995).
Gene_expression (detected) of GPe
15) Confidence 0.04 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0 Pain Relevance 0.19
Low levels of dopamine (Pifl et al., 1990) as well as DAT immunoreactivity and DAT ligand binding have also been detected in postmortem studies on human GPe tissue (Ciliax et al., 1999; Porritt et al., 2005) and rodent GP, the rodent homologue of the primate GPe (Ciliax et al., 1995; Coulter et al., 1995) indicating the presence of terminals of a dopaminergic projection in the GPe.
Gene_expression (projection) of GPe associated with dopamine
16) Confidence 0.04 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0 Pain Relevance 0.27
Low levels of dopamine (Pifl et al., 1990) as well as DAT immunoreactivity and DAT ligand binding have also been detected in postmortem studies on human GPe tissue (Ciliax et al., 1999; Porritt et al., 2005) and rodent GP, the rodent homologue of the primate GPe (Ciliax et al., 1995; Coulter et al., 1995) indicating the presence of terminals of a dopaminergic projection in the GPe.
Gene_expression (tissue) of GPe associated with dopamine
17) Confidence 0.04 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0 Pain Relevance 0.25
These D2LR-preferring agents may not only act in the striatum, but also at the level of the GPe or its afferents, and perhaps at glutamatergic synapses in GPi and SNr (see above).
Gene_expression (level) of GPe in synapses
18) Confidence 0.04 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0.30 Pain Relevance 0.27
For example, studies have reported decreased levels of dynorphin-like immunoreactivity in the striatum and globus pallidus (Haber et al 1986; Haber and Wolfer 1992), decreased subcortical levels of serotonin (Anderson et al 1992), increased numbers of neurons expressing parvalbumin in the globus pallidus pars internus (GPi) and decreased numbers of neurons expressing parvalbumin in the caudate nucleus and globus pallidus pars externus (GPe) (Kalanithi et al 2005).
Gene_expression (expressing) of GPe in caudate nucleus associated with dynorphin and serotonin
19) Confidence 0.04 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2646643 Disease Relevance 0.86 Pain Relevance 0.17
Hence, it can be concluded that the GPe may be one of the many cell groups, including the basal forebrain, thalamus, lateral hypothalamus, LC, and VTA, that directly modulate cortical activity.


Gene_expression (one) of GPe in forebrain associated with thalamus
20) Confidence 0.03 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.32 Pain Relevance 0.53

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