INT6588

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Context Info
Confidence 0.09
First Reported 1992
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 3
Total Number 3
Disease Relevance 0.53
Pain Relevance 1.04

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 (Nmt1) transferase activity, transferring acyl groups (Nmt1) cellular_component (Nmt1)
biological_process (Nmt1) cytoplasm (Nmt1)
Anatomy Link Frequency
neurons 1
Nmt1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
conotoxin 4 100.00 Very High Very High Very High
antagonist 1 100.00 Very High Very High Very High
Calcium channel 6 99.92 Very High Very High Very High
Glutamate receptor 1 99.56 Very High Very High Very High
gABA 3 98.52 Very High Very High Very High
Desipramine 1 94.92 High High
tetrodotoxin 1 88.44 High High
Hippocampus 2 84.80 Quite High
noradrenaline 2 83.32 Quite High
Clonidine 4 81.00 Quite High
Disease Link Frequency Relevance Heat
Convulsion 53 89.36 High High
Epilepsy 28 86.60 High High
Shock 2 55.64 Quite High
Anxiety 6 5.00 Very Low Very Low Very Low
Dizziness 6 5.00 Very Low Very Low Very Low
Generalized Epilepsy 5 5.00 Very Low Very Low Very Low
Learning Disorders 4 5.00 Very Low Very Low Very Low
Headache 4 5.00 Very Low Very Low Very Low
Sleep Disorders 3 5.00 Very Low Very Low Very Low
Aggression 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Ligands for L-type voltage-sensitive Ca2+ channels (VSCC) did not affect the evoked [3H]NA release, whereas the preferential N-type VSCC antagonist omega-conotoxin was inhibitory, both in the presence and even more potently in the absence of Ca2+, suggesting an involvement of N-type VSCC in the mechanism of 3,4-DAP-evoked [3H]NA release.
Negative_regulation (inhibitory) of N-type associated with antagonist and conotoxin
1) Confidence 0.09 Published 1992 Journal Eur. J. Pharmacol. Section Abstract Doc Link 1330632 Disease Relevance 0 Pain Relevance 0.51
In contrast, the N-type VOCC blocker, omega-conotoxin GVIA (omega-CgTx GVIA) (0.1-100 nM), markedly reduced the K(+)-evoked response, with maximal inhibition of approximately 60+/-8%. omega-Agatoxin IVA (omega-Aga IVA) (1-50 nM), which binds P-type and, at high doses, also Q-type VOCCs, produced dose-dependent inhibition of up to 25+/-3%, while the maximal inhibition observed with the non-selective VOCCs ligand, omega-conotoxin MVIIC (omega-CmTx MVIIC) (1 nM-3 microM), amounted to 85+/-8%.
Negative_regulation (reduced) of N-type associated with conotoxin
2) Confidence 0.04 Published 2001 Journal Neurochem. Int. Section Abstract Doc Link 11137631 Disease Relevance 0 Pain Relevance 0.18
Levetiracetam has no inhibitory effect on sodium or low-voltage-activated, T-type calcium channels in rat neocortical neurons12 and does not have a high affinity for GABA, N-methyl d-aspartate (NMDA) or glutamate receptors.6,7,11 Levetiracetam reduces high-voltage, N-type, calcium channel currents in isolated rat CA1 hippocampal neurons but does not have an effect on L-type, P-type or Q-type calcium channels.13,14 This effect occurs within a few seconds and suggests a direct interaction of levetiracetam with the N-type channel, rather than a second messenger pathway.
Negative_regulation (reduces) of N-type in neurons associated with gaba, glutamate receptor and calcium channel
3) Confidence 0.01 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2747386 Disease Relevance 0.53 Pain Relevance 0.34

General Comments

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