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a(CHEBI:dopamine)

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Entity

Name
dopamine
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 13

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Nicotinic Acetylcholine Receptors and Nicotinic Cholinergic Mechanisms of the Central Nervous System v1.0.0

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

Neural Systems Governed by Nicotinic Acetylcholine Receptors: Emerging Hypotheses v1.0.0

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

Naturally-expressed nicotinic acetylcholine receptor subtypes v1.0.0

Structural and functional properties of prefibrillar α-synuclein oligomers v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Discriminative Stimulus Properties of S(−)-Nicotine: “A Drug for All Seasons v1.0.0

Caenorhabditis elegans models of tauopathy v1.0.0

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

In-Edges 46

a(CHEBI:"kynurenic acid") decreases a(CHEBI:dopamine, loc(GO:"extracellular region")) View Subject | View Object

Activation of alpha7 nAChRs is known to contribute to the regulation of extracellular dopamine levels in the rat striatum (81). Application via microdialysis of KYNA or alpha-BGT to the rat striatum significantly reduces the extracellular levels of dopamine, and the magnitude of the effect of either antagonist alone is comparable to that of both antagonists together (285). PubMed:19126755

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MeSH
Corpus Striatum
Text Location
Review

a(CHEBI:nicotine) increases sec(a(CHEBI:dopamine)) View Subject | View Object

However, in rodent and nonprimate animal models, nicotine has been shown to enhance striatal dopamine release and to prevent toxin-induced degeneration of dopaminergic neurons (384, 385). PubMed:19126755

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MeSH
Corpus Striatum
Text Location
Review

a(HBP:"alpha-Bungarotoxin") decreases a(CHEBI:dopamine, loc(GO:"extracellular region")) View Subject | View Object

Activation of alpha7 nAChRs is known to contribute to the regulation of extracellular dopamine levels in the rat striatum (81). Application via microdialysis of KYNA or alpha-BGT to the rat striatum significantly reduces the extracellular levels of dopamine, and the magnitude of the effect of either antagonist alone is comparable to that of both antagonists together (285). PubMed:19126755

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Annotations
MeSH
Corpus Striatum
Text Location
Review

a(MESH:"7-chlorothiokynurenic acid") causesNoChange a(CHEBI:dopamine, loc(GO:"extracellular region")) View Subject | View Object

In contrast, the NMDA receptor antagonist 7-chloro-KYNA has no significant ef- fect on the extracellular levels of dopamine in the rat striatum (391). PubMed:19126755

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MeSH
Corpus Striatum
Text Location
Review

bp(GO:"neuronal action potential") increases sec(a(CHEBI:dopamine)) View Subject | View Object

Activation of somatodendritic alpha7 nAChRs increases the action potential-dependent release of dopamine, while activation of presynaptic alpha6 and/or alpha4 nAChRs increases action potential-independent dopamine release. PubMed:19126755

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Text Location
Review

act(p(HGNC:CHRNA7)) regulates a(CHEBI:dopamine, loc(GO:"extracellular region")) View Subject | View Object

Activation of alpha7 nAChRs is known to contribute to the regulation of extracellular dopamine levels in the rat striatum (81). Application via microdialysis of KYNA or alpha-BGT to the rat striatum significantly reduces the extracellular levels of dopamine, and the magnitude of the effect of either antagonist alone is comparable to that of both antagonists together (285). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

act(p(HGNC:CHRNA7)) increases a(CHEBI:dopamine, loc(GO:"extracellular region")) View Subject | View Object

As illustrated in Figure 8, KYNA-induced reduction of extracellular dopamine levels can be explained by the inhibition of tonically active alpha7 nAChRs in the dopaminergic neurons within the VTA and/or in cortical glutamatergic terminals that synapse onto striatal neurons. VTA dopaminergic neurons represent the major dopaminergic input to the nucleus accumbens. PubMed:19126755

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Annotations
MeSH
Dopaminergic Neurons
Text Location
Review

p(HBP:"alpha-4-containing nAChR") increases sec(a(CHEBI:dopamine)) View Subject | View Object

Activation of somatodendritic alpha7 nAChRs increases the action potential-dependent release of dopamine, while activation of presynaptic alpha6 and/or alpha4 nAChRs increases action potential-independent dopamine release. PubMed:19126755

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Text Location
Review

p(HBP:"alpha-6-containing nAChR") increases sec(a(CHEBI:dopamine)) View Subject | View Object

Activation of somatodendritic alpha7 nAChRs increases the action potential-dependent release of dopamine, while activation of presynaptic alpha6 and/or alpha4 nAChRs increases action potential-independent dopamine release. PubMed:19126755

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Annotations
Text Location
Review

composite(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) increases sec(a(CHEBI:dopamine)) View Subject | View Object

Perfusion of soluble Abeta into mouse prefrontal cortex increases dopamine secretion through a mechanism that is blocked by alpha7 antagonists (Wu et al., 2007). PubMed:19293145

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Annotations
MeSH
Prefrontal Cortex

a(CHEBI:"nicotinic acetylcholine receptor agonist") increases sec(a(CHEBI:dopamine)) View Subject | View Object

Exogenously applied nicotinic agonists enhance and nicotinic antagonists often diminish the release of ACh, dopamine (DA), norepinephrine, and serotonin, as well as glutamate and GABA. PubMed:17009926

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a(CHEBI:"nicotinic antagonist") decreases sec(a(CHEBI:dopamine)) View Subject | View Object

Exogenously applied nicotinic agonists enhance and nicotinic antagonists often diminish the release of ACh, dopamine (DA), norepinephrine, and serotonin, as well as glutamate and GABA. PubMed:17009926

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a(CHEBI:nicotine) decreases sec(a(CHEBI:dopamine)) View Subject | View Object

Nicotine decreases tonic DA release in the striatum that is evoked by single action potentials (127), and nicotine also alters the frequency dependence of DA release that is electrically evoked by stimulus trains (130, 131). PubMed:17009926

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Annotations
Cell Ontology (CL)
neuron
MeSH
Corpus Striatum

bp(GO:"action potential") increases sec(a(CHEBI:dopamine)) View Subject | View Object

Nicotine decreases tonic DA release in the striatum that is evoked by single action potentials (127), and nicotine also alters the frequency dependence of DA release that is electrically evoked by stimulus trains (130, 131). PubMed:17009926

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Annotations
Cell Ontology (CL)
neuron
MeSH
Corpus Striatum

a(CHEBI:"calcium(2+)") increases tloc(a(CHEBI:dopamine), fromLoc(GO:intracellular), toLoc(GO:"extracellular region")) View Subject | View Object

Stimulation of nicotinic receptors present at the CNS presynaptic neuronal membrane leads to an increase in presynaptic Ca2+ concentration, which may facilitate the release of a number of neurotransmitters, such as glutamate, GABA, dopamine, serotonin, norepinephrine, as well as ACh PubMed:26813123

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Annotations
MeSH
Synapses

p(MGI:Chrm4) decreases tloc(a(CHEBI:dopamine), fromLoc(GO:intracellular), toLoc(GO:"extracellular region")) View Subject | View Object

Corroborating this hypothesis, it has been demonstrated that dopamine efflux is increased in the nucleus accumbens of M4 knockout mice PubMed:26813123

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MeSH
CA3 Region, Hippocampal

p(HGNC:CHRM2) decreases act(a(CHEBI:dopamine)) View Subject | View Object

M2 mAChR is expressed throughout the brain, including the hippocampus and neocortex, and is abundant in non-cholinergic neurons that project to these areas. In the caudate-putamen, M2 mAChR acts as an inhibitory modulator on dopaminergic terminals[46-48]. PubMed:24590577

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MeSH
Neostriatum

a(CHEBI:nicotine) decreases a(CHEBI:dopamine) View Subject | View Object

For instance, dopamine increases in the extended amygdala during stress, fear, and nicotine withdrawal (Inglis and Moghaddam, 1999; Pape, 2005; Grace et al., 2007; Gallagher et al., 2008; Koob, 2009; Marcinkiewcz et al., 2009) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Amygdala

a(CHEBI:nicotine) increases tloc(a(CHEBI:dopamine), fromLoc(MESH:"Presynaptic Terminals"), toLoc(GO:"extracellular region")) View Subject | View Object

Chronic nicotine upregulates alpha4* nAChRs in dopaminergic presynaptic terminals, apparently leading to increased resting dopamine release from those terminals PubMed:21482353

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Presynaptic Terminals

bp(MESH:"Stress, Physiological") increases a(CHEBI:dopamine) View Subject | View Object

For instance, dopamine increases in the extended amygdala during stress, fear, and nicotine withdrawal (Inglis and Moghaddam, 1999; Pape, 2005; Grace et al., 2007; Gallagher et al., 2008; Koob, 2009; Marcinkiewcz et al., 2009) PubMed:21482353

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Annotations
MeSH
Amygdala

path(MESH:Fear) increases a(CHEBI:dopamine) View Subject | View Object

For instance, dopamine increases in the extended amygdala during stress, fear, and nicotine withdrawal (Inglis and Moghaddam, 1999; Pape, 2005; Grace et al., 2007; Gallagher et al., 2008; Koob, 2009; Marcinkiewcz et al., 2009) PubMed:21482353

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Annotations
MeSH
Amygdala

a(CHEBI:nicotine) regulates sec(a(CHEBI:dopamine)) View Subject | View Object

Nicotine facilitates dopamine release by acting at both somatodendritic and presynaptic nAChRs on mesolimbic246,247 and nigrostriatal247 neurons. PubMed:19721446

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Text Location
Review

act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) increases sec(a(CHEBI:dopamine)) View Subject | View Object

Typically, activation of brain nAChRs results in enhanced release of various key neurotransmitters, including dopamine, serotonin, glutamate and GABA (gamma-aminobutyric acid). PubMed:19721446

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Text Location
Review

p(HGNC:CHRNA6) association sec(a(CHEBI:dopamine)) View Subject | View Object

There is an emerging consensus that nAChR a6 subunit mRNA and proteins are distributed in brain regions thought to be involved in reward and drug reinforcement, in theory being involved in DA release [135]. PubMed:21787755

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MeSH
Brain

r(HGNC:CHRNA6) association sec(a(CHEBI:dopamine)) View Subject | View Object

There is an emerging consensus that nAChR a6 subunit mRNA and proteins are distributed in brain regions thought to be involved in reward and drug reinforcement, in theory being involved in DA release [135]. PubMed:21787755

Appears in Networks:
Annotations
MeSH
Brain

p(MGI:Dyrk1a) decreases a(CHEBI:dopamine) View Subject | View Object

DYRK1A overexpression induced dramatic deficits in the serotonin contents of the four brain areas tested and major deficits in dopamine and adrenaline contents especially in the hypothalamus. PubMed:28540658

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Annotations
Uberon
hypothalamus

a(CHEBI:nicotine) increases sec(a(CHEBI:dopamine)) View Subject | View Object

Moreover, (-)-nicotine (indirectly) can produce a release of dopamine in brain regions that are thought to control pleasure and motivation; dopamine is thought to underlie the pleasurable sensations experienced by smokers (e.g., [14, 15] but see [16]). PubMed:28391535

Appears in Networks:
Annotations
MeSH
Brain

a(CHEBI:nicotine) increases act(a(CHEBI:dopamine)) View Subject | View Object

For example, (-)-nicotine may increase dopamine activity at some brain sites such as the nucleus accumbens, an area thought to be important to drugs of abuse (e.g., [14, 101, 102]; but see [16, 103]) PubMed:28391535

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MeSH
Nucleus Accumbens

p(HGNC:DDC) increases a(CHEBI:dopamine) View Subject | View Object

A recent addition to the suppressors of tau-induced toxicity in C. elegans is the bas-1 gene (105), encoding the dopa decarboxylase, loss of which reduces the dopamine and serotonin levels (128–130). PubMed:29191965

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p(HGNC:GCH1) regulates a(CHEBI:dopamine) View Subject | View Object

Loss of function in other genes (cat-2, cat-4, tph-1) that also regulate the dopamine or serotonin levels (130–132),did not affect the tau-induced toxicity in TauV337M; however, their activity is essential for bas-1-mediated suppression of tau-induced toxicity in TauV337M (105) PubMed:29191965

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p(HGNC:TH) regulates a(CHEBI:dopamine) View Subject | View Object

Loss of function in other genes (cat-2, cat-4, tph-1) that also regulate the dopamine or serotonin levels (130–132),did not affect the tau-induced toxicity in TauV337M; however, their activity is essential for bas-1-mediated suppression of tau-induced toxicity in TauV337M (105) PubMed:29191965

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p(HGNC:TPH1) regulates a(CHEBI:dopamine) View Subject | View Object

Loss of function in other genes (cat-2, cat-4, tph-1) that also regulate the dopamine or serotonin levels (130–132),did not affect the tau-induced toxicity in TauV337M; however, their activity is essential for bas-1-mediated suppression of tau-induced toxicity in TauV337M (105) PubMed:29191965

Appears in Networks:

a(CHEBI:methamphetamine) decreases a(CHEBI:dopamine, loc(MESH:"Nerve Endings")) View Subject | View Object

Such an abnormal DA release produces peaks of extracellular DA, which cannot be taken up within nerve terminals, because METH inhibits and reverts the direction of the dopamine transporter (DAT). PubMed:30061532

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a(CHEBI:methamphetamine) decreases sec(a(CHEBI:dopamine)) View Subject | View Object

These findings strongly suggest that an autophagy dysfunction acts both at pre- and post-synaptic level to alter DA neurotransmission during both METH administration and schizophrenia (Figure 2) PubMed:30061532

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a(CHEBI:methamphetamine) increases a(CHEBI:dopamine, loc(GO:cytosol)) View Subject | View Object

In fact, METH produces a massive increase of endogenous intra-cytosolic DA levels by inhibiting and reverting the direction of the vesicular monoamine transporter type 2 (VMAT-2), thus disrupting the physiological storage of DA PubMed:30061532

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a(CHEBI:methamphetamine) association sec(a(CHEBI:dopamine)) View Subject | View Object

In line with this, experimental models of DISC1 deficiency treated with METH show a significant potentiation of DA release, along with increased expression of D1R in the ventral striatum when compared with controls PubMed:30061532

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bp(GO:autophagy) decreases sec(a(CHEBI:dopamine)) View Subject | View Object

Noteworthy, genetic ablation of autophagy was shown to produce an extremely powerful DA release upon electrical stimuli, suggesting that autophagy is key to restrain DA release both upon basal neural activity and mostly after rapamycin-induced autophagy PubMed:30061532

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bp(GO:autophagy) decreases sec(a(CHEBI:dopamine)) View Subject | View Object

These findings strongly suggest that an autophagy dysfunction acts both at pre- and post-synaptic level to alter DA neurotransmission during both METH administration and schizophrenia (Figure 2) PubMed:30061532

Appears in Networks:
Annotations
MeSH
Schizophrenia

act(complex(p(HGNC:ERBB4), p(HGNC:NRG1))) increases sec(a(CHEBI:dopamine)) View Subject | View Object

Noteworthy, NRG1/ErbB4 signaling plays a key role in DA-related behaviors by increasing DA release within the hippocampus, striatum, and prefrontal cortex PubMed:30061532

Appears in Networks:
Annotations
MeSH
Corpus Striatum
MeSH
Hippocampus
MeSH
Prefrontal Cortex

p(HGNC:DISC1, var("?")) decreases sec(a(CHEBI:dopamine)) View Subject | View Object

In addition, these findings strongly suggest that DISC1 alterations may increase the risk of schizophrenia by dysregulating DA release PubMed:30061532

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p(HGNC:SLC18A2) association a(CHEBI:dopamine) View Subject | View Object

In fact, METH produces a massive increase of endogenous intra-cytosolic DA levels by inhibiting and reverting the direction of the vesicular monoamine transporter type 2 (VMAT-2), thus disrupting the physiological storage of DA PubMed:30061532

Appears in Networks:

p(HGNC:SLC6A3) increases a(CHEBI:dopamine, loc(MESH:"Nerve Endings")) View Subject | View Object

Such an abnormal DA release produces peaks of extracellular DA, which cannot be taken up within nerve terminals, because METH inhibits and reverts the direction of the dopamine transporter (DAT). PubMed:30061532

Appears in Networks:

path(MESH:Schizophrenia) positiveCorrelation a(CHEBI:dopamine) View Subject | View Object

Accordingly, clinical evidence points towards an elevation of pre-synaptic DA synthesis and release as a key event for schizophrenia PubMed:30061532

Appears in Networks:

path(MESH:Schizophrenia) association sec(a(CHEBI:dopamine)) View Subject | View Object

Accordingly, clinical evidence points towards an elevation of pre-synaptic DA synthesis and release as a key event for schizophrenia PubMed:30061532

Appears in Networks:

path(MESH:Schizophrenia) increases a(CHEBI:dopamine) View Subject | View Object

Likewise, the psychostimulant effects experienced by METH-addicted patients rely on increased DA synthesis and massive DA release from nerve terminals within limbic areas as occurring in the schizophrenic brain PubMed:30061532

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Annotations
MeSH
Brain

path(MESH:Schizophrenia) increases tloc(a(CHEBI:dopamine), fromLoc(MESH:"Nerve Endings"), toLoc(MESH:"Limbic System")) View Subject | View Object

Likewise, the psychostimulant effects experienced by METH-addicted patients rely on increased DA synthesis and massive DA release from nerve terminals within limbic areas as occurring in the schizophrenic brain PubMed:30061532

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Annotations
MeSH
Brain

Out-Edges 13

a(CHEBI:dopamine) decreases path(MESH:"Parkinson Disease") View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
Text Location
Review

sec(a(CHEBI:dopamine)) association r(HGNC:CHRNA6) View Subject | View Object

There is an emerging consensus that nAChR a6 subunit mRNA and proteins are distributed in brain regions thought to be involved in reward and drug reinforcement, in theory being involved in DA release [135]. PubMed:21787755

Appears in Networks:
Annotations
MeSH
Brain

sec(a(CHEBI:dopamine)) association p(HGNC:CHRNA6) View Subject | View Object

There is an emerging consensus that nAChR a6 subunit mRNA and proteins are distributed in brain regions thought to be involved in reward and drug reinforcement, in theory being involved in DA release [135]. PubMed:21787755

Appears in Networks:
Annotations
MeSH
Brain

a(CHEBI:dopamine) increases a(HBP:HBP00093) View Subject | View Object

The neurotransmitter dopamine (DA) has been shown to promote the formation of stable, SDS-resistant α -syn oligomers both in vitro and in neurons30–32 by different mechanisms, including the formation of stable α -syn-DA-quinone adducts, methionine oxidation, or non-covalent interactions33. PubMed:27075649

Appears in Networks:
Annotations
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Lewy Bodies

a(CHEBI:dopamine) increases a(HBP:HBP00093) View Subject | View Object

DA-mediated α -syn oligomers constitute a range of SDS-resistant species with apparent molecular weights ranging from over 2200 to 200 kDa as determined by SEC (Fig. 4a). PubMed:27075649

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Annotations
MeSH
Intracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Lewy Bodies

a(CHEBI:dopamine) regulates path(MESH:Pleasure) View Subject | View Object

Moreover, (-)-nicotine (indirectly) can produce a release of dopamine in brain regions that are thought to control pleasure and motivation; dopamine is thought to underlie the pleasurable sensations experienced by smokers (e.g., [14, 15] but see [16]). PubMed:28391535

Appears in Networks:
Annotations
MeSH
Brain

a(CHEBI:dopamine) regulates path(MESH:Motivation) View Subject | View Object

Moreover, (-)-nicotine (indirectly) can produce a release of dopamine in brain regions that are thought to control pleasure and motivation; dopamine is thought to underlie the pleasurable sensations experienced by smokers (e.g., [14, 15] but see [16]). PubMed:28391535

Appears in Networks:
Annotations
MeSH
Brain

a(CHEBI:dopamine) positiveCorrelation path(MESH:Schizophrenia) View Subject | View Object

Accordingly, clinical evidence points towards an elevation of pre-synaptic DA synthesis and release as a key event for schizophrenia PubMed:30061532

Appears in Networks:

sec(a(CHEBI:dopamine)) association path(MESH:Schizophrenia) View Subject | View Object

Accordingly, clinical evidence points towards an elevation of pre-synaptic DA synthesis and release as a key event for schizophrenia PubMed:30061532

Appears in Networks:

a(CHEBI:dopamine) regulates bp(GO:autophagy) View Subject | View Object

In line with this, METH produces ultrastructural alterations reflecting dysfunctional autophagy flux, which are DA-dependent PubMed:30061532

Appears in Networks:

a(CHEBI:dopamine) association p(HGNC:SLC18A2) View Subject | View Object

In fact, METH produces a massive increase of endogenous intra-cytosolic DA levels by inhibiting and reverting the direction of the vesicular monoamine transporter type 2 (VMAT-2), thus disrupting the physiological storage of DA PubMed:30061532

Appears in Networks:

a(CHEBI:dopamine) increases bp(GO:"response to oxidative stress") View Subject | View Object

It is worth mentioning that freely diffusible intra-cytosolic DA can readily undergo auto-oxidation and produce a cascade of oxidative-related damage, which is bound to the neurotoxic effects of high doses of METH PubMed:30061532

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sec(a(CHEBI:dopamine)) association a(CHEBI:methamphetamine) View Subject | View Object

In line with this, experimental models of DISC1 deficiency treated with METH show a significant potentiation of DA release, along with increased expression of D1R in the ventral striatum when compared with controls PubMed:30061532

Appears in Networks:

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.