INT249306

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Context Info
Confidence 0.43
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 0.93
Pain Relevance 0.91

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

transport (Preb) vesicle-mediated transport (Preb) endoplasmic reticulum (Preb)
nucleus (Preb) DNA binding (Preb)
Anatomy Link Frequency
neurons 4
neuronal 1
Preb (Mus musculus)
Pain Link Frequency Relevance Heat
depression 102 99.92 Very High Very High Very High
Neuronal excitability 30 99.00 Very High Very High Very High
Action potential 12 96.40 Very High Very High Very High
Spinal cord 36 89.84 High High
medulla 84 89.36 High High
gABA 36 77.52 Quite High
agonist 30 75.60 Quite High
adenocard 66 75.00 Quite High
Glutamate 6 63.76 Quite High
Serotonin 6 62.08 Quite High
Disease Link Frequency Relevance Heat
Depression 108 99.92 Very High Very High Very High
Convulsion 36 95.12 Very High Very High Very High
Hypoxia 30 71.72 Quite High
Stress 12 48.32 Quite Low
Rheumatoid Arthritis 18 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Within the island preparation antagonism of GABAA and glycine receptors appeared to synchronize preBötC bursting, increasing burst amplitude [34].
Positive_regulation (synchronize) of preB
1) Confidence 0.43 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2567986 Disease Relevance 0.10 Pain Relevance 0
These findings, are consistent with the notion that the modulatory effects of A1R activation, although likely to integrate with concurrent synaptic inputs, are greater in their overall effect on preBötC activity than are A1R-induced changes in the net synaptic input to preBötC neurons from sources originating outside the preBötC.
Positive_regulation (effect) of preB in neurons
2) Confidence 0.43 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2567986 Disease Relevance 0.06 Pain Relevance 0
Depression of respiratory rhythmogenesis by A1R may be mediated by its effects on membrane properties, such as increasing conductance of leak K+ channels in preBötC neurons [24].
Positive_regulation (conductance) of preB in neurons associated with depression
3) Confidence 0.43 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2567986 Disease Relevance 0.34 Pain Relevance 0.37
In this study A1R activation depressed preBötC rhythmogenesis by acting directly on the preBötC within slice and island preparations, even though the frequency of synaptic currents in preBötC neurons is extensively reduced in the latter preparation.
Positive_regulation (activation) of preB in neurons
4) Confidence 0.40 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2567986 Disease Relevance 0.08 Pain Relevance 0.09
Thus, the data presented herein do not rule out the possibility that A1R activation may depress preBötC rhythmogenesis by directly inhibiting excitatory transmission between preBötC neurons.
Positive_regulation (activation) of preB in neurons
5) Confidence 0.40 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2567986 Disease Relevance 0.20 Pain Relevance 0.23
Together these data support the suggestion that depression of preBötC activity by A1R activation involves both decreased neuronal excitability and diminished inter-neuronal communication.



Positive_regulation (activation) of preB in neuronal associated with neuronal excitability and depression
6) Confidence 0.40 Published 2008 Journal BMC Neurosci Section Abstract Doc Link PMC2567986 Disease Relevance 0.15 Pain Relevance 0.23

General Comments

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