INT325697

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Context Info
Confidence 0.59
First Reported 2010
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 1
Total Number 5
Disease Relevance 0.12
Pain Relevance 1.50

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

cytosol (Aacs) ligase activity (Aacs) lipid metabolic process (Aacs)
cytoplasm (Aacs)
Anatomy Link Frequency
pyramidal cell 1
interneurons 1
Aacs (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 120 100.00 Very High Very High Very High
Action potential 60 99.56 Very High Very High Very High
Pyramidal cell 280 98.60 Very High Very High Very High
Endocannabinoid 20 82.08 Quite High
addiction 10 80.04 Quite High
depression 75 69.52 Quite High
Neurotransmitter 5 63.44 Quite High
agonist 20 59.72 Quite High
GABAergic 60 54.40 Quite High
Cholecystokinin 30 43.72 Quite Low
Disease Link Frequency Relevance Heat
Depression 75 69.52 Quite High
Targeted Disruption 15 5.00 Very Low Very Low Very Low
Cognitive Disorder 5 5.00 Very Low Very Low Very Low
Volume Depletion And Dehydration 5 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
By reducing the GABA release from the axon terminals of both AACs and FSBCs, carbachol accelerated the decay of uIPSCs recorded only in AAC– but not in FSBC–pyramidal cell pairs.
Localization (release) of AACs in pyramidal cell associated with gaba and pyramidal cell
1) Confidence 0.59 Published 2010 Journal The European Journal of Neuroscience Section Body Doc Link PMC2916217 Disease Relevance 0 Pain Relevance 0.38
We then examined the possibility of asynchronous release at the other two types of perisomatic inhibitory cell, but we did not find any significant change in the charge transfer following action potential trains tested at 30 Hz (P=0.17 for FSBCs, n=17; and P=0.05 for AACs, n=18), confirming that neither FSBCs nor AACs release transmitter in an asynchronous manner.
Neg (neither) Localization (release) of AACs associated with action potential
2) Confidence 0.59 Published 2010 Journal The European Journal of Neuroscience Section Body Doc Link PMC2916217 Disease Relevance 0 Pain Relevance 0.33
In the former case, the activation of M2-type muscarinic receptors located at the axon endings of FSBCs and AACs control GABA release (present study; Hajos et al., 1998; Fukudome et al., 2004).
Localization (release) of AACs associated with gaba
3) Confidence 0.51 Published 2010 Journal The European Journal of Neuroscience Section Body Doc Link PMC2916217 Disease Relevance 0 Pain Relevance 0.27
This mechanism allows the axon endings of FSBCs (and probably of AACs as well) to release GABA upon action potential discharge with high probability and with precise timing.
Localization (release) of AACs associated with action potential and gaba
4) Confidence 0.51 Published 2010 Journal The European Journal of Neuroscience Section Body Doc Link PMC2916217 Disease Relevance 0.12 Pain Relevance 0.23
These results indicate that, in contrast to FSBCs and AACs, RSBCs can release GABA asynchronously; the magnitude of this release increases with the firing frequency of the interneurons and this type of release is also suppressed by cholinergic receptor activation.


Localization (release) of AACs in interneurons associated with gaba
5) Confidence 0.30 Published 2010 Journal The European Journal of Neuroscience Section Body Doc Link PMC2916217 Disease Relevance 0 Pain Relevance 0.30

General Comments

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