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  • Title: Tumor necrosis factor-alpha impairs the recovery of synaptic transmission from hypoxia in rat hippocampal slices.
    Author: Batti L, O'Connor JJ.
    Journal: J Neuroimmunol; 2010 Jan 25; 218(1-2):21-7. PubMed ID: 19942300.
    Abstract:
    Cerebral ischaemia is a common occurrence in a range of pathological conditions, including stroke and traumatic brain injury. Two of the components in ischaemia are tissue hypoxia and the release of pro-inflammatory agents such as TNF-alpha. The role of TNF-alpha in an ischaemic/hypoxic episode is still controversial, although deleterious effects of pro-inflammatory cytokines in the area of injury are well documented. One of the prime adaptive mechanisms in response to hypoxia is the cellular activation of adenosine 1 receptors (A1Rs), which inhibits excitatory synaptic transmission. In the present study we have examined the effect of TNF-alpha application on synaptic transmission during hypoxic exposure and re-oxygenation using extracellular recordings in the CA1 region of the rat hippocampal slice. Hypoxia caused a reversible depression of the field EPSP (29.6+/-9.7% of control, n=5), which was adenosine A(1) receptor-dependent (85.7+/-4.3%, in the presence of DPCPX (200 nM), the adenosine A(1) receptor antagonist). DPCPX inhibited the maintenance of long-term potentiation obtained 30 min post hypoxia (143.8+/-8.2% versus 96.4+/-10.6% respectively, 1h post tetanus; n=5; p<0.005). In TNF-alpha (150 pM) treated slices hypoxic depression was similar to controls but a reduction in fEPSP slope was observed during re-oxygenation (66.8+/-1.4%, n=5). This effect was reversed by pre-treatment with SB 203580 (1 microM), a p38 MAP kinase inhibitor (91.8+/-6.9%, n=5). These results demonstrate a novel p38 MAPK dependent role for TNF-alpha in attenuating synaptic transmission after a hypoxic episode.
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