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