In the present study, we compare the effects on synaptic transmission of different experimental inflammatory models, LPS, a potent trigger of cytokine induction [19, 20] and the most common stimulus used to investigate microglial reactivity in brain inflammation, and a pro-inflammatory cocktail containing interleukin-1β (IL-1β), well-known determinant of neuropathy [1, 2], tumor necrosis factor α (TNF-α), present during Th1/Th17-mediated inflammatory reactions, and granulocyte macrophage-colony stimulating factor (GM-CSF), targeting resident microglial cells. The gene discussed is TNF; the disease is neuropathy.