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glial cell

Name
glial cell
Namespace Keyword
Cell
Namespace
Cell Ontology (CL)
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/cell/cell-20170511.belanno

Sample Annotated Edges 5

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

path(MESH:D000544) decreases bp(GO:"GO:0014047") View Subject | View Object

Second, because of this background signal, as well as the fact that neurons are left with smaller amounts of neurotransmitter to release into the synapse during neuronal firing, the 'peak signal'—the difference between synaptic glutamate concentration during neuronal activity and synaptic glutamate concentration under resting conditions—is attenuated, leading to suboptimal neurotransmission as exemplified by a lack of long-term potentiation (LTP) PubMed:16273023

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

bp(GO:"GO:0014047") increases bp(MESH:D017774) View Subject | View Object

Second, because of this background signal, as well as the fact that neurons are left with smaller amounts of neurotransmitter to release into the synapse during neuronal firing, the 'peak signal'—the difference between synaptic glutamate concentration during neuronal activity and synaptic glutamate concentration under resting conditions—is attenuated, leading to suboptimal neurotransmission as exemplified by a lack of long-term potentiation (LTP) PubMed:16273023

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

path(MESH:D000544) decreases bp(GO:"GO:0051935") View Subject | View Object

In patients with Alzheimer's disease, available evidence points to a disruption in the glutamatergic neurotransmission cycle at the point of glial cell reuptake of free glutamate from the synapse. Neuropathologic studies have documented reduced levels of glutamate reuptake in the frontal and temporal cortices of patients with Alzheimer's disease,10 possibly due to oxidative modification of the glutamate transporter 1 molecule. Furthermore, diminished uptake by vesicular glutamate transporter has been reported in patients with Alzheimer's disease PubMed:16273023

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

a(CHEBI:glutamine) increases bp(GO:"GO:0006868") View Subject | View Object

Synaptic glutamate concentration is promptly restored to normal levels, however, through the rapid uptake of unbound glutamate molecules by nearby glial cells, which subsequently convert these glutamate molecules to glutamine. The resulting glutamine molecules are then recycled to the neurons, and the cycle of glutamatergic signaling begins anew PubMed:16273023

Appears in Networks:
Annotations
Cell Ontology (CL)
glial cell

Showing 5 of 19 edges

About

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.