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Background Chronic pain in response to tissue inflammation (inflammatory pain) or nerve injury (neuropathic pain) is often unresponsive to currently available treatments. A large body of evidence indicates that production of nitric oxide (NO) and activation of NO-sensitive guanylyl cyclase (NO-GC) essentially contributes to the processing of chronic pain. NO-GC is a heterodimer consisting of one a subunit (a1 or a2) and one b1 subunit and exists in two isoforms (NO-GC1 and NOGC2). However, the functional role of NO-GC1 and NO-GC2 in pain processing remains poorly understood. Here, we investigated the expression of NO-GC isoforms in pain-relevant tissues (dorsal root ganglia and the spinal cord) and characterized the nociceptive behavior of mice lacking a1 or a2 in models of acute nociceptive, inflammatory and neuropathic pain.

Functions of NO-GC1 and NO-GC2 in pain processing