Brain natriuretic peptide (BNP) expressing sensory neurons are not involved in acute, inflammatory or neuropathic pain.

Background: We recently demonstrated that brain natriuretic peptide is expressed in the dorsal root ganglia, and that brain natriuretic peptide is required for normal detection of pruritogens. We further showed that the receptor for brain natriuretic peptide, natriuretic peptide receptor A, is present in the spinal cord, and elimination of these neurons profoundly attenuates scratching to itch-inducing compounds. However, the potential modulatory roles of brain natriuretic peptide in nociception, inflammation, and neuropathic mechanisms underlying the sensation of pain have not been investigated in detail. Findings: To demonstrate the involvement of brain natriuretic peptide in pain, we compared the behavioral responses of brain natriuretic peptide knockout mice with their wild-type littermates. First, we showed that brain natriuretic peptide is not required in chemically induced pain responses evoked by the administration of capsaicin, allyl isothiocyanate, adenosine 5′-triphosphate, or inflammatory soup. We further measured pain behaviors and found no involvement of brain natriuretic peptide in hot, cold, or mechanical nociceptive responses in mice, nor did we find evidence for the involvement of brain natriuretic peptide in neuroinflammatory sensitization elicited by complete Freund’s adjuvant or in neuropathic pain. Conclusions: These results demonstrate that brain natriuretic peptide is not essential for pain-related behaviors.