INT56461

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Context Info
Confidence 0.59
First Reported 1993
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 23
Total Number 24
Disease Relevance 2.03
Pain Relevance 20.74

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

cytoplasm (Vta1)
Anatomy Link Frequency
nucleus accumbens 3
ventral 3
shell 1
neurons 1
striatum 1
Vta1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 1194 100.00 Very High Very High Very High
Ventral tegmentum 980 100.00 Very High Very High Very High
Dynorphin 22 100.00 Very High Very High Very High
Glutamate 81 99.98 Very High Very High Very High
monoamine 74 99.98 Very High Very High Very High
Enkephalin 13 99.98 Very High Very High Very High
Substantia nigra 31 99.80 Very High Very High Very High
agonist 85 99.66 Very High Very High Very High
Nicotine 867 99.62 Very High Very High Very High
addiction 144 99.46 Very High Very High Very High
Disease Link Frequency Relevance Heat
Generalized Anxiety Disorder 38 99.76 Very High Very High Very High
Drug Dependence 88 96.32 Very High Very High Very High
Depression 7 95.08 Very High Very High Very High
Recurrence 15 94.60 High High
Urological Neuroanatomy 17 94.40 High High
Syndrome 14 93.00 High High
Hypothermia 8 89.56 High High
Parkinson's Disease 4 86.04 High High
Primary Sclerosing Cholangitis 19 83.76 Quite High
Sprains And Strains 2 54.96 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The continued survival of mesolimbic dopamine cell bodies after a 6-OHDA lesion may have functional implications relating to drugs of abuse, as somatodendritic release of dopamine in the VTA has been shown to play a role in the effectiveness of cocaine reward.
Localization (release) of VTA associated with ventral tegmentum, dopamine and cocaine
1) Confidence 0.59 Published 2002 Journal Neuroscience Section Abstract Doc Link 12453497 Disease Relevance 0.30 Pain Relevance 0.56
The functional integrity of the ventral tegmental area (VTA) is critical for these effects, which are mediated, at least in part, by nicotinic acetylcholine receptors located on dopamine (DA) neurons in the VTA.
Localization (located) of VTA in ventral associated with ventral tegmentum and dopamine
2) Confidence 0.53 Published 2008 Journal Brain Struct Funct Section Body Doc Link PMC2522332 Disease Relevance 0.09 Pain Relevance 0.62
Accordingly, dopamine release in the projection region of VTA neurons, the nucleus accumbens, would also increase.
Localization (release) of VTA in nucleus accumbens associated with nucleus accumbens, ventral tegmentum and dopamine
3) Confidence 0.48 Published 2002 Journal Eur. J. Neurosci. Section Abstract Doc Link 12099913 Disease Relevance 0.10 Pain Relevance 0.89
With the present study we demonstrate that while baclofen significantly reduces the electrically induced release of [3H]-DA from the VTA of saline-control rats, it has no effect on the evoked monoamine release from VTA slices of nicotine pre-treated rats.
Localization (release) of VTA associated with ventral tegmentum, dopamine, nicotine and monoamine
4) Confidence 0.46 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.91
The regulation of glutamate (Glu) release from the excitatory input to dopamine cells in the ventral tegmental area (VTA) during acute withdrawal from morphine was studied in slices from animals treated for 6-7 d with morphine.
Localization (release) of VTA in ventral associated with ventral tegmentum, dopamine, glutamate, withdrawal and morphine
5) Confidence 0.43 Published 1999 Journal J. Neurosci. Section Abstract Doc Link 10414991 Disease Relevance 0.05 Pain Relevance 1.00
M), added to the superfusion buffer 36 min before the second stimulation, dose-dependently reduced the electrically evoked [3H]-DA release from VTA slices (EC50 = 0.103 ?
Localization (release) of VTA associated with ventral tegmentum and dopamine
6) Confidence 0.43 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 1.10
The dissected VTA was cross-chopped (250 ?
Localization (dissected) of VTA associated with ventral tegmentum
7) Confidence 0.43 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0.05 Pain Relevance 0.25
Since GABAB receptors modulate the release of several neurotransmitters in the mammalian brain, we have characterised the effect of the GABAB receptor agonist baclofen on the release of [3H]-dopamine ([3H]-DA) from VTA slices of naïve rats and of rats pre-treated with nicotine.


Localization (release) of VTA in brain associated with ventral tegmentum, dopamine, neurotransmitter, nicotine and agonist
8) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Abstract Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.70
In naïve rats, baclofen concentration-dependently inhibited the electrically evoked release of [3H]-DA from the isolated VTA (EC50 = 0.103 ?
Localization (release) of VTA associated with ventral tegmentum
9) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Abstract Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.78
However, to date, there is a lack of information regarding the effect of GABAB receptor activation on the release of somatodendritic dopamine from the isolated VTA.
Localization (release) of VTA associated with ventral tegmentum and dopamine
10) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.77
In conclusion, we have demonstrated that activation of GABAB receptors inhibits the release of preloaded [3H]-DA from somatodendritic fields of VTA neurones in naïve rats.
Localization (release) of VTA associated with ventral tegmentum and dopamine
11) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.64
The effect of baclofen on the VTA [3H]-DA release in rats pre-treated with nicotine was assessed and compared with the effect of the drug in saline-control animals (Figure 6).
Localization (release) of VTA associated with ventral tegmentum, dopamine and nicotine
12) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.90
Not surprisingly, basal and evoked release of dopamine from VTA slices of rats chronically injected with nicotine did not differ from release obtained from saline-control tissue.
Localization (release) of VTA associated with ventral tegmentum, dopamine and nicotine
13) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.54
Tetrodotoxin and calcium dependence of the stimulated [3H]-DA release from VTA slices
Localization (release) of VTA associated with ventral tegmentum, addiction, tetrodotoxin and dopamine
14) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 1.52
Thus, if the GABAB receptors directly implicated in the control of dopamine release from the VTA represent only a small fraction of the overall receptor population in this area, autoradiographic analysis would not be sufficiently sensitive to evaluate receptor modifications occurring after chronic exposure to nicotine.
Localization (release) of VTA associated with ventral tegmentum, dopamine and nicotine
15) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.64
Our results demonstrate that GABAB receptor activation reduces the release of DA from the rat VTA.
Localization (release) of VTA associated with ventral tegmentum
16) Confidence 0.40 Published 2004 Journal BMC Pharmacol Section Abstract Doc Link PMC526276 Disease Relevance 0 Pain Relevance 0.88
We recently demonstrated that inhibition by URB597 of fatty acid amide hydrolase (FAAH), the main enzyme that degrades the endogenous cannabinoid N-acylethanolamine (NAE) anandamide and the endogenous non-cannabinoid NAEs oleoylethanolamide and palmitoylethanolamide, blocks nicotine-induced excitation of ventral tegmental area (VTA) dopamine (DA) neurons and DA release in the shell of the nucleus accumbens (ShNAc), as well as nicotine-induced drug self-administration, conditioned place preference and relapse in rats.
Localization (release) of VTA in shell associated with nucleus accumbens, ventral tegmentum, dopamine, nicotine, cannabinoid and recurrence
17) Confidence 0.34 Published 2010 Journal Addict Biol Section Abstract Doc Link 20477753 Disease Relevance 0.09 Pain Relevance 1.21
Importantly, the observed increase in GABAB heteroreceptor function would be expected to lead to decreased dopamine and glutamate release in the VTA, and may therefore contribute to the reward deficits associated with psychostimulant withdrawal (38).
Localization (release) of VTA associated with ventral tegmentum, glutamate, dopamine and withdrawal
18) Confidence 0.19 Published 2008 Journal Evidence-based Complementary and Alternative Medicine : eCAM Section Body Doc Link PMC2529396 Disease Relevance 0 Pain Relevance 1.37
These authors proposed that activation of serotonin neurons in the hypothalamus induces met-enkephalin release in the VTA, and as a consequence, GABA neurons in the VTA are inhibited, thereby increasing dopamine release in the nucleus accumbens (69).
Localization (release) of VTA in nucleus accumbens associated with nucleus accumbens, ventral tegmentum, dopamine, gaba, enkephalin and serotonin
19) Confidence 0.19 Published 2008 Journal Evidence-based Complementary and Alternative Medicine : eCAM Section Body Doc Link PMC2529396 Disease Relevance 0.14 Pain Relevance 1.53
The dopamine released from the dendrites [75, 76] might interact with dopamine D2 receptors localized on somata and/or dendrites of VTA neurons.
Localization (localized) of VTA in neurons associated with ventral tegmentum and dopamine
20) Confidence 0.12 Published 2004 Journal Purinergic Signal Section Body Doc Link PMC2096569 Disease Relevance 0 Pain Relevance 0.57

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