• Pablo Andrade, Veerle Visser-Vandewalle, Carolin Hoffmann, Harry W M Steinbusch, Marc A Daemen, and Govert Hoogland.
• Department of Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, Universiteitssingel 50, Box 38, 6200 MD Maastricht, The Netherlands. p.andrade@maastrichtuniversity.nl
• Neurol. Sci. 2011 Oct 1;32(5):757-71.

AbstractTumor necrosis factor-alpha (TNF-α) is a principal mediator in pro-inflammatory processes that involve necrosis, apoptosis and proliferation. Experimental and clinical evidence demonstrate that peripheral nerve injury results in activation and morphological changes of microglial cells in the spinal cord. These adjustments occur in order to initiate an inflammatory cascade in response to the damage. Between the agents involved in this reaction, TNF-α is recognized as a key player in this process as it not only modulates lesion formation, but also because it is suggested to induce nociceptive signals. Nowadays, even though the function of TNF-α in inflammation and pain production seems to be generally accepted, diverse sources of literature point to different pathways and outcomes. In this review, we systematically searched and reviewed original articles from the past 10 years on animal models of peripheral nervous injury describing TNF-α expression in neural tissue and pain behavior.

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