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Context Info
Confidence 0.68
First Reported 1983
Last Reported 1995
Negated 0
Speculated 0
Reported most in Abstract
Documents 10
Total Number 10
Disease Relevance 1.08
Pain Relevance 2.20

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

Anatomy Mention Frequency
urinary bladder 1
NG108-15 1
brain 1
forebrain 1
motor nerve 1


Pain Term Frequency Confidence Heat
tetrodotoxin 17 99.76 Very High Very High Very High
cerebral cortex 6 99.68 Very High Very High Very High
sodium channel 2 97.84 Very High Very High Very High
antagonist 1 92.60 High High
depression 1 90.56 High High
substance P 3 88.00 High High
Enkephalin 1 87.52 High High
Somatostatin 1 85.84 High High
Clonidine 1 83.52 Quite High
Morphine 1 82.32 Quite High
Disease Term Frequency Confidence Heat
Urological Neuroanatomy 9 99.28 Very High Very High Very High
Poisoning 1 93.64 High High
Neuroblastoma 1 91.36 High High
Depression 1 90.56 High High
Glioma 1 90.56 High High
Shock 2 76.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The external calcium-independent ACh release induced by CTX in motor terminals seems to be due to a Na(+)-dependent and tetrodotoxin-sensitive mechanism which mobilizes Ca2+ from intraterminal stores, as determined by fluorometrical recordings in single mouse neuroblastoma x rat glioma NG108-15 cells.
Localization (release) of ACh in NG108-15 associated with tetrodotoxin, neuroblastoma and glioma
1) Confidence 0.68 Published 1992 Journal Bull Soc Pathol Exot Section Abstract Doc Link 1340351 Disease Relevance 0.18 Pain Relevance 0.10
Addition of either tetrodotoxin, pilocarpine, or methoctramine had no effect on honokiol-enhanced ACh release.
Localization (release) of ACh associated with tetrodotoxin
2) Confidence 0.68 Published 1995 Journal Planta Med. Section Abstract Doc Link 7480213 Disease Relevance 0 Pain Relevance 0.10
It was concluded that neurotensin stimulated ACh release via a neurogenic mechanism, probably by a presynaptic site of action on myenteric cholinergic neurons.
Localization (release) of ACh in cholinergic neurons
3) Confidence 0.68 Published 1983 Journal Eur. J. Pharmacol. Section Abstract Doc Link 6140179 Disease Relevance 0 Pain Relevance 0.21
These findings suggest that the urinary bladder of the rat is equipped with presynaptic inhibitory muscarinic receptors modulating ACh release from cholinergic postganglionic neurons.
Localization (release) of ACh in urinary bladder
4) Confidence 0.68 Published 1986 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 3772807 Disease Relevance 0.14 Pain Relevance 0.07
A factor (Substance B) has been isolated from brain which reverses the presynaptically-modulated inhibition of evoked ACh release from both guinea-pig myenteric plexus-longitudinal muscle synaptosomes and the intact strip.
Localization (release) of ACh in brain
5) Confidence 0.68 Published 1986 Journal J. Physiol. (Paris) Section Abstract Doc Link 3572823 Disease Relevance 0 Pain Relevance 0.20
In the frontal cortex, NT significantly inhibited evoked ACh release by a tetrodotoxin (TTX)-insensitive mechanism, suggesting an action directly on cholinergic terminals.
Localization (release) of ACh in frontal cortex associated with tetrodotoxin and urological neuroanatomy
6) Confidence 0.68 Published 1990 Journal J. Neurochem. Section Abstract Doc Link 2144584 Disease Relevance 0.19 Pain Relevance 0.32
The second set of experiments tested the effects of quinolinic acid (QUIN) lesions of the basal forebrain cell bodies on the NT-induced regulation of evoked ACh release in the cerebral cortex.
Localization (release) of ACh in cerebral cortex associated with cerebral cortex
7) Confidence 0.68 Published 1990 Journal J. Neurochem. Section Abstract Doc Link 2144584 Disease Relevance 0.20 Pain Relevance 0.32
The results show that NT differentially regulates evoked ACh release from frontal and parietal cortex slices without altering either spontaneous or evoked ACh release from basal forebrain slices.
Localization (release) of ACh in forebrain
8) Confidence 0.68 Published 1990 Journal J. Neurochem. Section Abstract Doc Link 2144584 Disease Relevance 0.19 Pain Relevance 0.28
These findings suggest the involvement of the three neurokinin (NK) receptors in ACh release evoked by TKs with the following rank order: NK3 greater than NK2 greater than NK1. 6-Hydroxydopamine lesions of nigrostriatal neurons and tetrodotoxin (TTX) intoxication of striatal tissue revealed two different patterns of regulation of cholinergic function by TKs.
Localization (release) of ACh in neurons associated with tetrodotoxin and poisoning
9) Confidence 0.68 Published 1991 Journal J. Neurosci. Section Abstract Doc Link 1651375 Disease Relevance 0.09 Pain Relevance 0.38
We conclude that aconitine increases and then decreases electrical stimulation-evoked ACh release from the motor nerve through prolonged activation of sodium channels.
Localization (release) of ACh in motor nerve associated with sodium channel
10) Confidence 0.68 Published 1994 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 7723217 Disease Relevance 0.09 Pain Relevance 0.22

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