INT261511

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Context Info
Confidence 0.02
First Reported 2007
Last Reported 2007
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 15
Disease Relevance 5.06
Pain Relevance 7.27

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

small molecule metabolic process (CBS) lyase activity (CBS) enzyme binding (CBS)
cytoplasm (CBS) cytosol (CBS) nucleolus (CBS)
Anatomy Link Frequency
DA neurons 6
neuronal 2
dorsal 1
CBS (Homo sapiens)
Pain Link Frequency Relevance Heat
Dopamine 1245 100.00 Very High Very High Very High
Ventral tegmentum 240 99.84 Very High Very High Very High
addiction 225 99.84 Very High Very High Very High
Glutamate 180 98.80 Very High Very High Very High
gABA 75 98.28 Very High Very High Very High
depression 90 98.12 Very High Very High Very High
ischemia 75 97.84 Very High Very High Very High
Nucleus accumbens 90 97.48 Very High Very High Very High
GABAergic 150 96.80 Very High Very High Very High
withdrawal 15 94.00 High High
Disease Link Frequency Relevance Heat
Drug Dependence 165 99.84 Very High Very High Very High
Injury 90 99.32 Very High Very High Very High
Epilepsy 15 98.44 Very High Very High Very High
Depression 90 98.12 Very High Very High Very High
Cv Unclassified Under Development 75 97.84 Very High Very High Very High
Recurrence 45 96.76 Very High Very High Very High
Stroke 45 96.72 Very High Very High Very High
Disease 465 95.60 Very High Very High Very High
Stress 75 94.04 High High
Death 60 90.08 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Studies in our laboratory provided evidence that eCBs released by DA neurons exert protective actions in a model of ischemia/reperfusion [137].
Localization (released) of eCBs in DA neurons associated with dopamine and ischemia
1) Confidence 0.02 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.53 Pain Relevance 0.31
In fact, the eCBs released by VTA DA neurons, by moving retrogradely toward presynaptic CB1 receptors located on both glutamatergic and GABAergic terminals [136, 138, 161, 219], finely adjust the balance between excitatory and inhibitory synaptic inputs, thus contributing to the regulation of their own firing pattern and/or activity and, consequently, of the whole reward pathway.
Localization (released) of eCBs in DA neurons associated with ventral tegmentum, dopamine and gabaergic
2) Confidence 0.02 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.18 Pain Relevance 0.69
In addition, the findings that eCBs release and CB1 receptor activation are necessary for LTD in both the nucleus accumbens [162, 163] and the dorsal neostriatum [67-69] support their involvement in those behaviours mediating the crucial transition from the reward-dependent form of drug-taking to the compulsive one.
Localization (release) of eCBs in dorsal associated with nucleus accumbens and depression
3) Confidence 0.02 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.23 Pain Relevance 0.55
Thus, the finding that eCBs may be released during burst of DA neurons, similar to those caused by behaviourally salient events, appears particularly intriguing.
Localization (released) of eCBs in DA neurons associated with dopamine
4) Confidence 0.02 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0 Pain Relevance 0.55
One possibility is that eCBs released by VTA DA neurons might selectively regulate their own synaptic inputs depending upon the relative level of synaptic activation of the different pathways.
Localization (released) of eCBs in DA neurons associated with ventral tegmentum and dopamine
5) Confidence 0.02 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.36 Pain Relevance 0.81
But if this is the case, the most likely scenario is that SNc DA cells would release eCBs to dampen the hyperactivated corticostriatal glutamatergic transmission, a feature of experimental models of PD [19, 20, 23, 183].
Localization (release) of eCBs associated with dopamine and disease
6) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.92 Pain Relevance 0.33
Thus, one plausible speculation is that -once released by these DA cells- eCBs might act not only as neuroprotective but also as neurorescue molecules to provide protection against the progression of neuronal injury characteristic of PD.
Localization (released) of eCBs in neuronal associated with dopamine, injury and disease
7) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 1.05 Pain Relevance 0.27
The prediction that this depolarization would trigger the release of eCBs was confirmed by the finding that blockade of CB1 receptors induced a considerable worsening of the outcome of experimental ischemia [137].
Localization (release) of eCBs associated with ischemia
8) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.44 Pain Relevance 0.33
Under these circumstances, released eCBs transiently modulate presynaptically afferent activity and shape incoming inputs, thus inducing DSE or DSI [138, 161, 219].
Localization (released) of eCBs
9) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0 Pain Relevance 0.44
These stimuli induce a cascade of intracellular events ultimately leading to an increased intracellular Ca2+ and release of eCBs.
Localization (release) of eCBs
10) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0 Pain Relevance 0.44
It has been suggested that the release of eCBs during neuronal injury might be a protective response.
Localization (release) of eCBs in neuronal associated with injury
11) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.90 Pain Relevance 0.16
However, while the DA system appears to be involved more than others in the pathophysiology of addiction, the studies examining eCB actions in the reward pathway have not fully elucidated the mechanisms underlying their involvement in the several aspects of drug dependence (e.g.: eCBs released in the VTA and primary rewarding effects of diverse drugs of abuse; eCB role in relapse to drug-seeking behaviours).
Localization (released) of eCBs associated with drug dependence, ventral tegmentum, addiction, dopamine and recurrence
12) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.41 Pain Relevance 0.74
eCBs, released upon depolarization and/or receptor activation, can transiently affect synaptic efficacy by suppressing either GABA or glutamate release, thus provoking depolarization-induced suppression of inhibition (DSI) or excitation (DSE), respectively [1, 31, 48, 216]. eCBs can also affect other forms of short term synaptic transmission, which are induced by more physiologically relevant patterns of synaptic activity [15, 17, 136], and result in modulation of synaptic strength and/or firing pattern in vivo [10, 29, 136].
Localization (released) of eCBs associated with glutamate and gaba
13) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0.05 Pain Relevance 0.36
Under what circumstances DA neurons release eCBs?
Localization (release) of eCBs in DA neurons associated with dopamine
14) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0 Pain Relevance 0.58
This hypothesis was confirmed by patch-clamp experiments providing evidence that DA neurons release eCBs as retrograde messengers in a Ca2+-dependent manner.
Localization (release) of eCBs in DA neurons associated with dopamine
15) Confidence 0.01 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644494 Disease Relevance 0 Pain Relevance 0.71

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