Targeting tumour necrosis factor-α in hypoxia and synaptic signalling
|Title:||Targeting tumour necrosis factor-α in hypoxia and synaptic signalling||Authors:||O'Connor, J. J.||Permanent link:||http://hdl.handle.net/10197/4133||Date:||Jan-2013||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||Copyright (published version):||Royal Academy of Medicine in Ireland 2013||Keywords:||TNF-α;Hypoxia;Prolyl hydroxylase;Hippocampus;Synaptic transmission;Synaptic plasticity;Inflammation||DOI:||10.1007/s11845-013-0911-4||Language:||en||Status of Item:||Not peer reviewed|
|Appears in Collections:||Conway Institute Research Collection|
Biomolecular and Biomedical Science Research Collection
Show full item record
Page view(s) 20161
This item is available under the Attribution-NonCommercial-NoDerivs 3.0 Ireland. No item may be reproduced for commercial purposes. For other possible restrictions on use please refer to the publisher's URL where this is made available, or to notes contained in the item itself. Other terms may apply.