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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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Corpus Striatum
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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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Corpus Striatum
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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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Corpus Striatum
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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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Corpus Striatum
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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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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

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Corpus Striatum
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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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MeSH
Dopaminergic Neurons
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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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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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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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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

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

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

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

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

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

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

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

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

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

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

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

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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.