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Appears in Networks 5

In-Edges 10

a(CHEBI:"nicotinic acetylcholine receptor agonist") increases sec(a(CHEBI:serotonin)) 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:serotonin)) 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:"calcium(2+)") increases tloc(a(CHEBI:serotonin), 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

a(MESH:"Receptors, Nicotinic") regulates sec(a(CHEBI:serotonin)) View Subject | View Object

Also, α7- and non-α7-containing nicotinic receptors directly or indirectly (through GABAergic interneurons) modulate serotonin release in spinal cord slices230. However, the identity of the receptors that are responsible for the spinal control of nociception is currently unknown. in this process, the nicotine-induced antinociception seems to be mediated primarily by activation of calcium– calmodulin-dependent protein kinase 2, but this is not the case for supraspinal nociception control229. PubMed:19721446

act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) increases sec(a(CHEBI:serotonin)) 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(MGI:Dyrk1a) decreases a(CHEBI:serotonin) 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

p(HGNC:DDC) increases a(CHEBI:serotonin) 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:serotonin) 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:serotonin) 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:serotonin) 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

Out-Edges 0

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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.