Received May 4, 2005
Revised May 31, 2005
Accepted after revision June 7, 2005
Actions of TNF-
on glutamatergic synaptic transmission in the central nervous sysyem
Mark Pickering 1,
Derval Cumiskey 1,
John J. O'Connor 1*
1 University College Dublin
* To whom correspondence should be addressed. E-mail: john.oconnor{at}ucd.ie.
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Abstract |
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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-
(TNF-) is a pro-inflammatory cytokine the receptors for which are expressed on neurons 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- has direct effects on glutamate transmission, for example increasing expression of AMPA receptors on synapses. TNF- also plays a role in synaptic plasticity, inhibiting long term potentiation (LTP), a process dependant on p38 MAP kinase. In the following review we look at these and other effects of TNF- in the CNS.
Key Words:
Cytokine, Glutamate, LTP
