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a(CHEBI:"glutamate(2-)")

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Entity

Name
glutamate(2-)
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 8

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

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

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

Interplay of neurotransmitters in Alzheimer's disease v1.0.0

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

In-Edges 14

a(MESH:"Mossy Fibers, Hippocampal") increases a(CHEBI:"glutamate(2-)", loc(MESH:"Pyramidal Cells")) View Subject | View Object

Activation of alpha7 nAChRs in somatodendritic and preterminal/ terminal areas of interneurons in various strata of the CA1 region and in the dentate gyrus facilitates spontaneous quantal release of GABA (14, 25). Glutamate release from mossy fibers onto CA3 pyramidal neurons is also modulated by alpha7 nAChRs present in the mossy fiber terminals (190). PubMed:19126755

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Annotations
MeSH
CA1 Region, Hippocampal
Text Location
Review

act(p(HGNC:CHRNA7, loc(GO:"glutamatergic synapse"))) increases a(CHEBI:"glutamate(2-)", loc(MESH:"Dopaminergic Neurons")) View Subject | View Object

Other levels of regulation of dopaminergic transmission arise from alpha7 nAChRs located on cortical glutamatergic terminals; activation of these receptors increases glutamate release onto dopaminergic neurons in the VTA and, consequently, increases the their firing (344). PubMed:19126755

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Text Location
Review

p(HGNC:CHRNA7, loc(MESH:"Mossy Fibers, Hippocampal")) regulates a(CHEBI:"glutamate(2-)", loc(MESH:"Pyramidal Cells")) View Subject | View Object

Activation of alpha7 nAChRs in somatodendritic and preterminal/ terminal areas of interneurons in various strata of the CA1 region and in the dentate gyrus facilitates spontaneous quantal release of GABA (14, 25). Glutamate release from mossy fibers onto CA3 pyramidal neurons is also modulated by alpha7 nAChRs present in the mossy fiber terminals (190). PubMed:19126755

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Annotations
MeSH
CA1 Region, Hippocampal
Text Location
Review

act(p(HGNC:CHRNA7)) decreases act(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Nicotinic neuroprotection against non-Abeta toxicity is also mediated largely through alpha7 nAChRs. alpha7 nAChRs protect PC12 cells against ethanol toxicity (Li et al., 1999a) and from cell death associated with serum depletion (Ren et al., 2005); they protect cultured neurons against glutamate-induced excitotoxicity (Kaneko et al., 1997) and hippocampal slices against oxygen and glucose deprivation (Egea et al., 2007) through the activation of alpha7 nAChRs (Rosa et al., 2006). PubMed:19293145

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Annotations
MeSH
Neurons

act(p(RGD:Chrna7)) decreases act(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Calcium signaling pathways are involved both in the toxic action of Abeta and in the protection against that toxicity offered by nicotinic ligands. Given that alpha7 homomeric nAChRs are much more permeable to calcium ions than are most other nAChRs (Bertrand et al., 1993), it is to be expected that nicotinic neuroprotection mediated by nAChRs, notably alpha7, would depend upon the activation of calcium signaling pathways. ABT-418 is a nicotinic agonist that protects primary rat cortical neurons from glutamate toxicity through its activation of alpha7 nAChRs, and this is blocked when calcium is removed from the extracellular medium (Donnelly-Roberts et al., 1996). PubMed:19293145

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a(CHEBI:"nicotinic acetylcholine receptor agonist") increases sec(a(CHEBI:"glutamate(2-)")) 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:"glutamate(2-)")) 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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act(p(HGNC:CHRNA7)) increases sec(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Postsynaptic β2∗ nAChRs initially depolarize DA neurons, causing them to fire action potentials while presynaptic α7∗ nAChRs boost glutamate release. PubMed:17009926

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Annotations
Cell Ontology (CL)
dopaminergic neuron
MeSH
Presynaptic Terminals

act(p(FPLX:CHRN)) increases sec(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Nicotinic stimulation enhances glutamate release on multiple timescales, extending from seconds to a few minutes (81), and contributes to the induction of synaptic plasticity (4, 13, 14, 16, 88). PubMed:17009926

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p(FPLX:CHRN) increases sec(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Presynaptic and preterminal nAChRs increase the release of neurotransmitters in the hippocampus, particularly the main neurotransmitters, GABA and glutamate (41, 78, 81, 97). PubMed:17009926

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Annotations
MeSH
Hippocampus
MeSH
Presynaptic Terminals

act(p(FPLX:CHRN)) increases sec(a(CHEBI:"glutamate(2-)")) View Subject | View Object

Activation of the presynaptic nAChRs (commonly but not exclusively α 7 * nAChRs) enhances the release of glutamate (Dani et al., 2000; Mansvelder & McGehee, 2000, 2002). PubMed:26472524

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Annotations
MeSH
Presynaptic Terminals

a(CHEBI:"calcium(2+)") increases tloc(a(CHEBI:"glutamate(2-)"), 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

a(CHEBI:"gamma-aminobutyric acid") decreases tloc(a(CHEBI:"glutamate(2-)"), fromLoc(GO:intracellular), toLoc(GO:"extracellular region")) View Subject | View Object

The neurons release additional GABA, activating presynaptic GABAB receptors on the excitatory inputs to pyramidal neurons, which diminish the release of glutamate onto the pyramidal neurons (Figure 2) PubMed:21482353

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Annotations
MeSH
Pyramidal Cells

act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) increases sec(a(CHEBI:"glutamate(2-)")) 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

Out-Edges 5

a(CHEBI:"glutamate(2-)", loc(MESH:"Dopaminergic Neurons")) increases bp(GO:"synaptic transmission, dopaminergic") View Subject | View Object

Other levels of regulation of dopaminergic transmission arise from alpha7 nAChRs located on cortical glutamatergic terminals; activation of these receptors increases glutamate release onto dopaminergic neurons in the VTA and, consequently, increases the their firing (344). PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

act(a(CHEBI:"glutamate(2-)")) increases bp(HBP:Excitotoxicity) View Subject | View Object

Nicotinic neuroprotection against non-Abeta toxicity is also mediated largely through alpha7 nAChRs. alpha7 nAChRs protect PC12 cells against ethanol toxicity (Li et al., 1999a) and from cell death associated with serum depletion (Ren et al., 2005); they protect cultured neurons against glutamate-induced excitotoxicity (Kaneko et al., 1997) and hippocampal slices against oxygen and glucose deprivation (Egea et al., 2007) through the activation of alpha7 nAChRs (Rosa et al., 2006). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Neurons

sec(a(CHEBI:"glutamate(2-)")) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

The combination of enhanced glutamatergic release and strong postsynaptic response produces LTP of the glutamatergic afferents. PubMed:17009926

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Annotations
Cell Ontology (CL)
glutamatergic neuron

a(CHEBI:"glutamate(2-)") directlyIncreases bp(GO:"GO:0014047") View Subject | View Object

In healthy individuals, the glutamatergic neurotransmission cycle begins in the mitochondria of hippocampal neurons, where the enzyme glutaminase catalyzes the conversion of glutamine to glutamate. Next, the vesicular glutamate transporter molecule mediates the packaging of these glutamate molecules into vesicles. Glutamate-containing vesicles are then released from the neuron, resulting in elevated synaptic concentrations of free glutamate, which can transmit neural signals by interacting with glutamatergic receptors on postsynaptic neurons PubMed:16273023

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Annotations
MeSH
Mitochondria
Cell Ontology (CL)
hippocampal neuron
MeSH
Hippocampus

a(CHEBI:"glutamate(2-)") directlyIncreases act(p(MESH:D017470)) View Subject | View Object

First, the presence of elevated neurotransmitter levels in the synapse under resting conditions can be thought of as a constant 'background signal,' leading to chronic low-level activation of glutamatergic receptors on postsynaptic neurons and possibly neuronal death. PubMed:16273023

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Cell Ontology (CL)
glial cell
Disease Ontology (DO)
Alzheimer's disease
MeSH
Frontal Lobe
MeSH
Temporal Lobe

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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.