Nociception in cyclooxygenase isozyme-deficient mice

摘要: Prostaglandins formed by cyclooxygenase-1 (COX-1) or COX-2 produce hyperalgesia in sensory nerve endings. To assess the relative roles of two enzymes pain processing, we compared responses COX-1- COX-2-deficient homozygous and heterozygous mice with wild-type controls hot plate stretching tests for analgesia. Preliminary observational studies determined that there were no differences gross parameters behavior between different groups. Surprisingly, on (55°C), COX-1-deficient groups showed less nociception, because mean reaction time was longer than controls. All other similar times. In test, nociception COX-1-null heterozygotes also, unexpectedly, female heterozygotes, as shown a decreased number writhes. Measurements mRNA levels reverse transcription–PCR demonstrated compensatory increase COX-1 spinal cords COX-2-null but animals. Thus, compensation absence may not involve increased expression COX-2, whereas up-regulation cord compensate COX-2. The times are difficult to explain, nonsteroid anti-inflammatory drugs have analgesic action this test. Reduction writhes be due low at site stimulation acetic acid. prostaglandins made mainly involved transmission test both male mice, those also play role response mice.