INT69763

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Context Info
Confidence 0.50
First Reported 1997
Last Reported 2010
Negated 0
Speculated 4
Reported most in Abstract
Documents 12
Total Number 16
Disease Relevance 9.05
Pain Relevance 12.46

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

aging (Cnr1) plasma membrane (Cnr1) response to stress (Cnr1)
signal transducer activity (Cnr1)
Anatomy Link Frequency
nerve 4
boutons 4
spinal cord dorsal horn 4
lateral columns 3
neuronal 2
Cnr1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Cannabinoid 131 100.00 Very High Very High Very High
alcohol 14 100.00 Very High Very High Very High
Cannabinoid receptor 10 100.00 Very High Very High Very High
Opioid 10 100.00 Very High Very High Very High
antinociception 7 100.00 Very High Very High Very High
Glutamate receptor 4 100.00 Very High Very High Very High
qutenza 93 99.80 Very High Very High Very High
Antinociceptive 8 99.70 Very High Very High Very High
Neuropathic pain 14 99.44 Very High Very High Very High
Central grey 92 99.22 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nervous System Injury 49 99.98 Very High Very High Very High
Anxiety Disorder 188 99.96 Very High Very High Very High
Neuropathic Pain 16 99.44 Very High Very High Very High
Spasticity 41 99.36 Very High Very High Very High
Urological Neuroanatomy 101 99.22 Very High Very High Very High
Recurrence 8 99.12 Very High Very High Very High
Hypothermia 4 97.68 Very High Very High Very High
Multiple Sclerosis 25 96.48 Very High Very High Very High
Pain 27 90.88 High High
Nociception 4 88.72 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We found that subchronic activation of CB1 (WIN 55,212-2, 2 mg/kg), but not D2 receptors (quinpirole, 1 mg/kg), during a period of alcohol deprivation increased long-lasting alcohol relapse.
Positive_regulation (increased) of Positive_regulation (activation) of CB1 associated with recurrence and alcohol
1) Confidence 0.50 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18554293 Disease Relevance 0.77 Pain Relevance 0.69
Here we investigated whether presynaptic inhibition can be caused by activation of postsynaptic group I metabotropic glutamate receptors (mGluRs) and following presynaptic cannabinoid receptor type 1 (CB1 receptor) using mechanically dissociated rat hippocampal CA3 pyramidal neurons with adherent functional synaptic boutons.
Positive_regulation (activation) of Positive_regulation (following) of cannabinoid receptor type 1 in boutons associated with cannabinoid receptor, pyramidal cell and glutamate receptor
2) Confidence 0.48 Published 2010 Journal Neuroscience Section Abstract Doc Link 19961906 Disease Relevance 0 Pain Relevance 0.81
Here we investigated whether presynaptic inhibition can be caused by activation of postsynaptic group I metabotropic glutamate receptors (mGluRs) and following presynaptic cannabinoid receptor type 1 (CB1 receptor) using mechanically dissociated rat hippocampal CA3 pyramidal neurons with adherent functional synaptic boutons.
Positive_regulation (activation) of Positive_regulation (activation) of CB1 receptor in boutons associated with cannabinoid receptor, pyramidal cell and glutamate receptor
3) Confidence 0.48 Published 2010 Journal Neuroscience Section Abstract Doc Link 19961906 Disease Relevance 0 Pain Relevance 0.81
The demonstration that APAP produces hypothermia independent of opioid, cannabinoid CB1 or NOP receptor activation is contrary to its antinociceptive effect, which requires opioid and cannabinoid CB1 receptor activation.
Positive_regulation (requires) of Positive_regulation (activation) of cannabinoid CB1 associated with hypothermia, paracetamol, cannabinoid, antinociceptive and opioid
4) Confidence 0.47 Published 2009 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 19463266 Disease Relevance 0.31 Pain Relevance 1.70
In the midbrain dorsolateral periaqueductal gray (dlPAG) our previous data showed that CB1 activation induces anxiolytic-like effects.
Positive_regulation (induces) of Positive_regulation (activation) of CB1 in midbrain associated with anxiety disorder, midbrain and central grey
5) Confidence 0.44 Published 2009 Journal Eur Neuropsychopharmacol Section Abstract Doc Link 19064314 Disease Relevance 0.49 Pain Relevance 0.46
However, recent studies using the cannabinoid receptor-selective antagonist SR141716A suggest that the central actions of psychoactive cannabinoids are mediated principally through activation of CB1 receptors.
Positive_regulation (mediated) of Positive_regulation (activation) of CB1 associated with cannabinoid receptor, cannabinoid and antagonist
6) Confidence 0.41 Published 1997 Journal Neurosci. Lett. Section Abstract Doc Link 9175591 Disease Relevance 0 Pain Relevance 0.93
At the intracellular level, the mitogen-activated protein kinase (ERK-MAPK) inhibitor PD98059 (1 microg) prevented, while the protein kinase C inhibitor chelerythrine (10 microg) partially reduced, the CCI-induced CB1R upregulation when each agent was administered intrathecally for postoperative days 1-6.
Positive_regulation (induced) of Positive_regulation (upregulation) of CB1R associated with nervous system injury and kinase c inhibitor
7) Confidence 0.37 Published 2003 Journal Pain Section Abstract Doc Link 14499445 Disease Relevance 1.17 Pain Relevance 0.87
dorsal and lateral columns induces antinociception via activation of CB1
Positive_regulation (induces) of Positive_regulation (activation) of CB1 in lateral columns associated with antinociception
8) Confidence 0.35 Published 2009 Journal Neural Plasticity Section Body Doc Link PMC2593468 Disease Relevance 0.70 Pain Relevance 0.82
they are being mediated by activation of CB1 receptors, possibly by presynaptic
Spec (possibly) Positive_regulation (mediated) of Positive_regulation (activation) of CB1
9) Confidence 0.35 Published 2009 Journal Neural Plasticity Section Body Doc Link PMC2593468 Disease Relevance 0.59 Pain Relevance 0.37
Since CB1 receptors appear to be located mainly presynaptically and inhibit calcium influx at axon terminals, they are ideally positioned to inhibit the release of classical neurotransmitters such as glutamate.2,3 Activation of CB1 receptors also decreases neuronal excitability by activating somatic and dendritic potassium channels.2 Using the experimental allergic encephalomyelitis (EAE) mouse model of MS, cannabinoids have been reported to reduce both spasticity and tremor; furthermore, changes in CB1 receptors have been found in the CNS of EAE animals.4–6 This has led to the proposal that endocannabinoids provide a natural, anti-spastic function in the CNS.7

Clinical trial evidence

Positive_regulation (located) of Positive_regulation (receptors) of CB1 in neuronal associated with endocannabinoid, spasticity, cannabinoid, tremor, neurotransmitter, glutamate, multiple sclerosis, neuronal excitability, potassium channel and experimental autoimmune encephalomyelitis
10) Confidence 0.26 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2835560 Disease Relevance 1.30 Pain Relevance 0.96
CCI induced a time-dependent upregulation of spinal CB1Rs primarily within the ipsilateral superficial spinal cord dorsal horn as revealed by both Western blot and immunohistochemistry.
Positive_regulation (induced) of Positive_regulation (upregulation) of CB1Rs in spinal cord dorsal horn associated with nervous system injury, dorsal horn and spinal cord
11) Confidence 0.22 Published 2003 Journal Pain Section Abstract Doc Link 14499445 Disease Relevance 0.93 Pain Relevance 0.70
Here, we examined the hypothesis that the upregulation of spinal CB1R induced by chronic constriction nerve injury (CCI) in rats would be regulated by spinal GR.
Spec (examined) Positive_regulation (induced) of Spec (examined) Positive_regulation (upregulation) of CB1R in nerve associated with nervous system injury
12) Confidence 0.15 Published 2007 Journal Pain Section Abstract Doc Link 17258396 Disease Relevance 0.63 Pain Relevance 0.45
Here, we examined the hypothesis that the upregulation of spinal CB1R induced by chronic constriction nerve injury (CCI) in rats would be regulated by spinal GR.
Spec (examined) Positive_regulation (upregulation) of Spec (examined) Positive_regulation (induced) of CB1R in nerve associated with nervous system injury
13) Confidence 0.15 Published 2007 Journal Pain Section Abstract Doc Link 17258396 Disease Relevance 0.63 Pain Relevance 0.45
CCI induced the upregulation of spinal CB1R primarily within the ipsilateral spinal cord dorsal horn as revealed by Western blot and immunohistochemistry.
Positive_regulation (induced) of Positive_regulation (upregulation) of CB1R in spinal cord dorsal horn associated with nervous system injury, dorsal horn and spinal cord
14) Confidence 0.15 Published 2007 Journal Pain Section Abstract Doc Link 17258396 Disease Relevance 0.69 Pain Relevance 0.47
This prolonged irreversible effect of CAP might be due to other mechanisms, such as CB1 activation.
Spec (might) Positive_regulation (due) of Positive_regulation (activation) of CB1 associated with qutenza
15) Confidence 0.14 Published 2006 Journal Mol Pain Section Body Doc Link PMC1434724 Disease Relevance 0.14 Pain Relevance 1.18
dorsal and lateral columns induces antinociception via activation of CB1
Positive_regulation (induces) of in dorsal Positive_regulation (activation) of CB1 in lateral columns associated with antinociception
16) Confidence 0.12 Published 2009 Journal Neural Plasticity Section Body Doc Link PMC2593468 Disease Relevance 0.70 Pain Relevance 0.82

General Comments

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