Functions of NO-GC1 and NO-GC2 in pain processing
BMC Pharmacology and Toxicology volume 16, Article number: A74 (2015)
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 α subunit (α1 or α2) and one β1 subunit and exists in two isoforms (NO-GC1 and NO-GC2). 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 α1 or α2 in models of acute nociceptive, inflammatory and neuropathic pain.
Our behavioral data point to different and partly contrary functions of NO-GC1 and NO-GC2 in the processing of inflammatory and neuropathic pain. The expression of NO-GC isoforms in dorsal root ganglia and the spinal cord is restricted to specific neuronal and non-neuronal cell populations. It remains to be determined which targets mediate the pain-relevant effects of NO-GC1 and NO-GC2.
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Petersen, J., Mergia, E., Drees, O. et al. Functions of NO-GC1 and NO-GC2 in pain processing. BMC Pharmacol Toxicol 16 (Suppl 1), A74 (2015). https://doi.org/10.1186/2050-6511-16-S1-A74