Chronic pain due to a variety of health conditions is the primary reason people seek medical care, yet current therapies either are inadequate or cause intolerable side effects. Understanding cellular and molecular processes that lead to the initiation and maintenance of chronic pain will give promise to the development of more effective, more specific pain therapies. Chronic pain is an expression of neuronal plasticity, which is mediated in part by increased excitability of nociceptive neurons in the dorsal horn of the spinal cord . The molecular mechanisms that underlie this nociceptive plasticity are not fully understood. In the spinal cord, Nitric Oxide (NO) is known to contribute to central mechanisms that induce hyperalgesia and allodynia . There is also convincing evidence that a downstream molecule of the NO-cyclic guanosine monophosphate (cGMP) signaling pathway, Protein Kinase G (PKG), is involved in spinal nociceptive processing . However, PKG phosphorylation targets in the spinal cord and their role in the central sensitization of chronic pain have not been elucidated.
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