Antinociceptive activities of non-steroidal antiinflammatory drugs (NSAIDs) following intracerebroventricular (i.c.v.) and intrathecal (i.t.) administration in mice

Analgesics of the non-steroidal antiinflammatory group (NSAID) are classified as "peripheral analgesics" and act via cyclooxygenase inhibition, reducing the biosynthesis of peripheral prostaglandins (PGs). However, there has been some evidence that NSAIDs also reduce the nociceptive and hyperalgesic stimuli, either via inhibition of central cyclooxygenase [1], or via inhibition of Substance P (SP), another known mediator of pain at the spinal level [2]. This study was undertaken to investigate whether the antinociceptive effects of NSAIDs in the phenylbenzoquinone (PBQ)-induced writhing assay in mice had a central component, at either a supraspinal or spinal site, and for their effect against intrathecally administered SP.