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Actions of TNF‐α on glutamatergic synaptic transmission in the central nervous system
Author(s) -
Pickering Mark,
Cumiskey Derval,
O'Connor John J.
Publication year - 2005
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2005.030734
Subject(s) - excitotoxicity , ampa receptor , neuroscience , neuroprotection , glutamate receptor , long term potentiation , synaptic plasticity , glutamatergic , neurotransmission , biology , central nervous system , long term depression , tumor necrosis factor alpha , receptor , immunology , biochemistry
Increasing attention is being paid to the role of inflammatory and immune molecules in the modulation of central nervous system (CNS) function. Tumour necrosis factor‐α (TNF‐α) is a pro‐inflammatory cytokine, the receptors for which are expressed on neurones and glial cells throughout the CNS. Through the action of its two receptors, it has a broad range of actions on neurones which may be either neuroprotective or neurotoxic. It plays a facilitatory role in glutamate excitotoxicity, both directly and indirectly by inhibiting glial glutamate transporters on astrocytes. Additionally, TNF‐α has direct effects on glutamate transmission, for example increasing expression of AMPA receptors on synapses. TNF‐α also plays a role in synaptic plasticity, inhibiting long‐term potentiation (LTP), a process dependent on p38 mitogen activated kinase (p38 MAP) kinase. In the following review we look at these and other effects of TNF‐α in the CNS.