E-type prostaglandins depolarize primary afferent neurons of the neonatal rat.
The mechanism of action of prostaglandins (PGs) to sensitize sensory terminals to noxious stimuli was studied in the isolated spinal cord-tail preparation of the newborn rat. Application of a small amount of capsaicin to the tail induced a nociceptive reflex that was recorded extracellularly from the lumbar ventral root. Pretreatment of the tail with PGE1 or E2 (0.8-4 microM) markedly potentiated the capsaicin-induced nociceptive reflex. In the isolated spinal cord preparation of the newborn rat, application of PGE1 or E2 (10 nM-1 microM) induced a depolarization of the dorsal root. Based on these results we propose a hypothesis that PGs regulate the resting potential of the peripheral terminals of nociceptive primary afferent fibers and that the depolarization is associated with lowering of threshold for various noxious stimuli.
D000818:Animals; D000831:Animals, Newborn; D002211:Capsaicin / Q000494:pharmacology*; D004357:Drug Synergism; D008564:Membrane Potentials / Q000187:drug effects; D009619:Nociceptors / Q000187:drug effects*; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats; D012018:Reflex / Q000187:drug effects*; D013623:Tail / Q000294:innervation
D011458:Prostaglandins E; D002211:Capsaicin