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bp(GO:"membrane depolarization")

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Entity

Name
membrane depolarization
Namespace
go
Namespace Version
20181221
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/73688d6dc24e309fca59a1340dc9ee971e9f3baa/external/go-names.belns

Appears in Networks 5

albuquerque2009 v1.0.0

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

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

Neuronal Nicotinic Acetylcholine Receptor Structure and Function and Response to Nicotine v1.0.1

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

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

In-Edges 9

act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) increases bp(GO:"membrane depolarization") View Subject | View Object

It has long been recognized that nAChR activation in mammalian sympathetic neurons induces the opening of a nonselective cation channel that leads to Na+ influx, membrane depolarization, and consequently activation of voltage-gated Ca2+ channels (92, 119). PubMed:19126755

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Text Location
Review

act(complex(GO:"GABA-A receptor complex")) increases bp(GO:"membrane depolarization") View Subject | View Object

In the rat CA3 region, spontaneous activation of GABA A receptors produces giant depolarizing potentials, whose frequency is controlled by α7∗ and non-α7 nAChRs. PubMed:17009926

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MeSH
CA3 Region, Hippocampal

act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

Nicotinic receptor activity causes depolarization, and the divalent cation perme- ability plays an important physiological role by supplying ionic signals, including calcium (39–41). PubMed:17009926

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act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

In addition, nAChR activity produces a depolarization that activates voltage-gated calcium channels in the presynaptic terminal (87). PubMed:17009926

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Annotations
MeSH
Presynaptic Terminals

act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

Activation of nAChRs on distal apical dendrites depolarizes the cell and promotes action potential firing PubMed:17009926

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Annotations
MeSH
Dendrites
MeSH
Neocortex

tloc(a(CHEBI:"calcium(2+)"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) increases bp(GO:"membrane depolarization") View Subject | View Object

While nAChR activity causes depolarization, the divalent cation permeability plays an impor- tant physiological role by supplying ionic signals, including calcium (Bertrand, Galzi, Devillers-Thiery, Bertrand, & Changeux, 1993b; Dani & Bertrand, 2007; Decker & Dani, 1990; Gray, Rajan, Radcliffe, Yakehiro, & Dani, 1996; McGehee, Heath, Gelber, Devay, & Role, 1995; Vernino et al., 1992). PubMed:26472524

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tloc(a(MESH:"Cations, Divalent"), fromLoc(MESH:"Extracellular Space"), toLoc(MESH:"Intracellular Space")) increases bp(GO:"membrane depolarization") View Subject | View Object

While nAChR activity causes depolarization, the divalent cation permeability plays an impor- tant physiological role by supplying ionic signals, including calcium (Bertrand, Galzi, Devillers-Thiery, Bertrand, & Changeux, 1993b; Dani & Bertrand, 2007; Decker & Dani, 1990; Gray, Rajan, Radcliffe, Yakehiro, & Dani, 1996; McGehee, Heath, Gelber, Devay, & Role, 1995; Vernino et al., 1992). PubMed:26472524

Appears in Networks:

act(p(FPLX:CHRN)) increases bp(GO:"membrane depolarization") View Subject | View Object

While nAChR activity causes depolarization, the divalent cation permeability plays an impor- tant physiological role by supplying ionic signals, including calcium (Bertrand, Galzi, Devillers-Thiery, Bertrand, & Changeux, 1993b; Dani & Bertrand, 2007; Decker & Dani, 1990; Gray, Rajan, Radcliffe, Yakehiro, & Dani, 1996; McGehee, Heath, Gelber, Devay, & Role, 1995; Vernino et al., 1992). PubMed:26472524

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act(complex(GO:"NF-kappaB complex")) decreases bp(GO:"membrane depolarization") View Subject | View Object

In primary neuronal cells, exposure to Aβ25-35 peptide increase NF-κB mediated transactivation of manganese superoxide dismutase (Mn-SOD), suppress peroxinitrite production and inhibit membrane depolarization, thereby preventing apoptosis induced by oxidative stress PubMed:25652642

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MeSH
Neurons
MeSH
Alzheimer Disease

Out-Edges 5

bp(GO:"membrane depolarization") increases act(complex(GO:"voltage-gated calcium channel complex")) View Subject | View Object

In addition, nAChR activity produces a depolarization that activates voltage-gated calcium channels in the presynaptic terminal (87). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Presynaptic Terminals

bp(GO:"membrane depolarization") regulates act(p(HGNC:CHAT)) View Subject | View Object

ChAT activity is regulated by neuronal depolarization, influx of Ca2+ and phosphorylation of the enzyme by a wide variety of protein kinases PubMed:26813123

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Annotations
MeSH
Neurons

bp(GO:"membrane depolarization") increases tloc(a(CHEBI:acetylcholine), fromLoc(MESH:"Synaptic Vesicles"), toLoc(GO:"synaptic cleft")) View Subject | View Object

When cholinergic neurons are depolarized, ACh is exocytosed from synaptic vesicles and released into the synaptic cleft, where it can activate both muscarinic and nicotinic receptors PubMed:26813123

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Annotations
Cell Ontology (CL)
cholinergic neuron

bp(GO:"membrane depolarization") increases complex(a(GO:"plasma membrane"), p(HGNC:SLC5A7)) View Subject | View Object

It is possible that the presence of CHT1 in the membrane of synaptic vesicles and the consequent increase in CHT1 relocation to the plasma membrane following neuronal depolarization could explain why an increase in neuronal firing promotes increased choline reuptake and, thus, ACh synthesis PubMed:26813123

Appears in Networks:
Annotations
MeSH
Neurons

bp(GO:"membrane depolarization") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

A number of physiological stimuli including membrane depolarization or glutamergic signal transduction lead to rapid activation of the inducible NF-κB localized in the synapses, cytoplasm and dendrites of the neurons PubMed:25652642

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Dendrites
MeSH
Neurons
MeSH
Synapses

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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.