Options
Targeting tumour necrosis factor-α in hypoxia and synaptic signalling
Author(s)
Date Issued
2013-01
Date Available
2014-01-31T04:00:08Z
Abstract
Tumour necrosis factor (TNF)-α is a pro-inflammatory cytokine, which is synthesised and released in the brain by astrocytes, microglia and neurons in response to numerous internal and external stimuli. It is involved in many physiological and pathophysiological processes such as gene transcription, cell proliferation, apoptosis, synaptic signalling and neuroprotection. The complex actions of TNF-α in the brain are under intense investigation. TNF-α has the ability to induce selective necrosis of some cells whilst sparing others and this has led researchers to discover multiple activated signalling cascades. In many human diseases including acute stroke and inflammation and those involving hypoxia, levels of TNF-α are increased throughout different brain regions. TNF-α signalling may also have several positive and negative effects on neuronal function including glutamatergic synaptic transmission and plasticity. Exogenous TNF-α may also exacerbate the neuronal response to hypoxia. This review will summarise the actions of TNF-α in the central nervous system on synaptic signalling and its effects during hypoxia.
Type of Material
Journal Article
Publisher
Springer-Verlag
Journal
Irish Journal of Medical Science
Issue
January 2013
Copyright (Published Version)
Royal Academy of Medicine in Ireland 2013
Language
English
Status of Item
Not peer reviewed
ISSN
0021-1265
1863-4362
This item is made available under a Creative Commons License
File(s)
Owning collection
Scopus© citations
34
Acquisition Date
Mar 19, 2024
Mar 19, 2024
Views
1733
Last Month
1
1
Acquisition Date
Mar 19, 2024
Mar 19, 2024
Downloads
677
Last Week
7
7
Last Month
15
15
Acquisition Date
Mar 19, 2024
Mar 19, 2024