“…Additionally, glia produce and release proinflammatory cytokines, including interleukin-1 (IL1), tumor necrosis factoralpha (TNF) and interleukin-6 (IL6) (Benveniste, 1997), that further stimulate glial cells and neurons (Halassa et al, 2007, Nguyen et al, 2002. In the CNS, astrocytes and microglia express receptors for IL1, TNF andIL6 (Halassa et al, 2007, Hanisch, 2002), and respond to these cytokines by releasing NO (Burgher et al, 1997, Murphy andGrzybycki, 1996), EAAs and prostaglandins (Halassa et al, 2007, Pocock andKettenmann, 2007), increasing substance P release from primary afferent neurons (Inoue et al, 1999), and by up-regulating enzymes such as cyclooxygenase-2 characterized to produce prostaglandins that facilitate pain transmission (Samad et al, 2001). Thus, understanding pain mechanisms from a perspective that includes spinal cord glial stimulation has contributed to our knowledge about potential mechanisms that underlie the shift from adaptive pain to pathological pain (DeLeo et al, 2007).…”