INT48120

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Context Info
Confidence 0.34
First Reported 1995
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 5
Disease Relevance 1.20
Pain Relevance 2.22

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

transport (Cacna1h) nucleus (Cacna1h) transmembrane transport (Cacna1h)
cytoplasm (Cacna1h)
Anatomy Link Frequency
neurons 1
thalamus 1
Cacna1h (Mus musculus)
Pain Link Frequency Relevance Heat
Calcium channel 10 99.96 Very High Very High Very High
Pain 8 99.82 Very High Very High Very High
Thalamus 4 98.92 Very High Very High Very High
tetrodotoxin 4 98.24 Very High Very High Very High
gABA 4 97.88 Very High Very High Very High
backache 1 94.44 High High
Fibrositis 1 94.00 High High
Myofascial pain syndrome 1 93.28 High High
Action potential 3 90.52 High High
antagonist 2 88.28 High High
Disease Link Frequency Relevance Heat
Neuropathic Pain 1 97.92 Very High Very High Very High
Acidosis 1 97.44 Very High Very High Very High
Myalgia 2 97.32 Very High Very High Very High
Alkalosis 1 96.92 Very High Very High Very High
Pain 3 95.24 Very High Very High Very High
Low Back Pain 1 94.68 High High
Sleep Disorders 1 94.00 High High
Myofascial Pain Syndromes 1 93.28 High High
Hyperalgesia 4 79.16 Quite High
Disease 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In contrast to high-voltage-activated calcium channels which can be activated by a strong depolarization of membrane potential, T-type channels can be activated by a weak depolarization near the resting membrane potential once deinactivated by hyperpolarization, and therefore can regulate the excitability and electroresponsiveness of neurons under physiological conditions near resting states.
Positive_regulation (activated) of T-type in neurons associated with calcium channel
1) Confidence 0.34 Published 2008 Journal Curr Opin Pharmacol Section Abstract Doc Link 18203662 Disease Relevance 0 Pain Relevance 0.14
The role of low-voltage activated T-type calcium channels during such forms of pathology as neuropathy, acidosis and alkalosis because the changes in synaptic transmission occurring during these forms of pathological changes are most intensively altered during changes in functional structures of these type of channels.
Positive_regulation (activated) of T-type associated with alkalosis, acidosis, calcium channel and neuropathic pain
2) Confidence 0.34 Published 2008 Journal Fiziol Zh Section Abstract Doc Link 18763584 Disease Relevance 0.29 Pain Relevance 0.20
The threshold for activation of the T-type Ca2+ current was 20 mV negative to that of the tetrodotoxin-sensitive Na+ current.
Positive_regulation (activation) of T-type Ca2 associated with tetrodotoxin
3) Confidence 0.07 Published 1995 Journal Am. J. Physiol. Section Abstract Doc Link 7503267 Disease Relevance 0 Pain Relevance 0.13
Ca(v)3.2 T-type Ca2+ channel-dependent activation of ERK in paraventricular thalamus modulates acid-induced chronic muscle pain.
Positive_regulation (activation) of T-type in thalamus associated with pain, thalamus and myalgia
4) Confidence 0.07 Published 2010 Journal J. Neurosci. Section Title Doc Link 20685979 Disease Relevance 0.91 Pain Relevance 1.17
No evidence was found for involvement of Cav1/alpha1C and alpha1D (L-type), Cav2.2/alpha1B (N-type) or Cav2.3/alpha1E (R-type) high-voltage-activated VDCCs or low-voltage-activated Cav3/alpha1G, alpha1H and alpha1I (T-type) VDCCs in mediating presynaptic GABA release.
Positive_regulation (low-voltage-activated) of alpha1H associated with gaba
5) Confidence 0.03 Published 2001 Journal Eur. J. Neurosci. Section Abstract Doc Link 11403683 Disease Relevance 0 Pain Relevance 0.58

General Comments

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