INT333518

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Context Info
Confidence 0.41
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 4
Disease Relevance 0.34
Pain Relevance 1.18

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 2
Substantia nigra pars compacta 1
GYPE (Homo sapiens)
Pain Link Frequency Relevance Heat
Dopamine 177 100.00 Very High Very High Very High
Substantia nigra 14 99.08 Very High Very High Very High
gABA 30 96.04 Very High Very High Very High
GABAergic 40 89.88 High High
sodium channel 2 72.96 Quite High
tetrodotoxin 2 71.12 Quite High
cerebral cortex 12 59.32 Quite High
antagonist 19 26.52 Quite Low
dopamine receptor 33 24.72 Low Low
Calcium channel 1 23.96 Low Low
Disease Link Frequency Relevance Heat
Attention Deficit Hyperactivity Disorder 11 99.32 Very High Very High Very High
Targeted Disruption 10 71.28 Quite High
Disease 144 5.00 Very Low Very Low Very Low
Parkinson's Disease 61 5.00 Very Low Very Low Very Low
Sleep Disorders 52 5.00 Very Low Very Low Very Low
Weight Loss 12 5.00 Very Low Very Low Very Low
Tremor 10 5.00 Very Low Very Low Very Low
Cognitive Disorder 7 5.00 Very Low Very Low Very Low
Body Weight 6 5.00 Very Low Very Low Very Low
Hypokinesia 5 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
One of the counterintuitive features of increasing the GPe to GPe inhibition is that it can increase the spread of activity through rebound.
Negative_regulation (inhibition) of GPe
1) Confidence 0.41 Published 2010 Journal Philosophical transactions. Series A, Mathematical, physical, and engineering sciences Section Body Doc Link PMC2944387 Disease Relevance 0 Pain Relevance 0
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.
Negative_regulation (loss) of GPe in neurons associated with gaba and attention deficit hyperactivity disorder
2) Confidence 0.07 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.17 Pain Relevance 0.39
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.
Negative_regulation (inhibition) of GPe in neurons associated with gaba and attention deficit hyperactivity disorder
3) Confidence 0.05 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2996256 Disease Relevance 0.17 Pain Relevance 0.38
Substantia nigra pars compacta lesions in rodents and monkeys reduce dopamine levels in GPe (Parent et al., 1990; Jan et al., 2000; Fuchs and Hauber, 2004).
Negative_regulation (reduce) of GPe in Substantia nigra pars compacta associated with dopamine and substantia nigra
4) Confidence 0.04 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2987554 Disease Relevance 0 Pain Relevance 0.41

General Comments

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