The role of nitric oxide and prostaglandin signaling pathways in spinal nociceptive processing in chronic inflammation

摘要: Both nitric oxide (NO) and prostaglandins (PG) their associated enzymes synthases (NOS) cyclooxygenases (COX) (specifically COX-2) have been implicated in the development of hyperalgesia. This study examined effects naturally occurring chronic inflammation, mastitis, on spinal nociceptive processing sheep focused potential alterations PG NO signaling pathways. Mechanical withdrawal thresholds were significantly lower animals suffering from inflammation (n=6) compared to control (n=6). Hyperalgesia was restricted side contralateral (decrease ipsilateral side: hindlimb 33.2±5%, forelimb 19.4±5%). Neuronal NOS-immunoreactivity reduced bilaterally lumbar cervical cord throughout laminae I–III 18.4±5% 16.9±4%, respectively) lamina X 29.1±6% 17.1±4%, mastitic relative animals. No difference detected eNOS or iNOS-immunoreactivity NADPH-diaphorase staining, a marker dynamically active NOS. RT-PCR failed detect any change levels nNOS, eNOS, iNOS, COX-1 COX-2 mRNAs. However, marked increase PGE receptor, EP3 (but not EP2) mRNA tissue with inflammation. receptor expression indicates that PGs are important response peripheral Contralateral mechanical hyperalgesia may be directly linked changes expression, however, bilateral nNOS suggest this pathway contribute adaptive behavioural observed.