Spinal administration of prostaglandin E2 or prostaglandin F2α primarily produces mechanical hyperalgesia that is mediated by nociceptive specific spinal dorsal horn neurons

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Abstract
The effects of intrathecal (i.t.) administration of prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) on behavioral and spinal neuronal responses to mechanical and thermal stimuli were examined in rats. i.t. Administration of either PGE2 (1–100 nmol) or PGF2α (1–100 nmol) produced a robust, dose-dependent mechanical hyperalgesia, but only a weak thermal hyperalgesia and touch-evoked allodynia. Spinal administration of either PGE2 (100 pmol–100 nmol) or PGF2α (1–100 nmol) produced dose-dependent increases in responses of nociceptive specific (NS) neurons to mechanical stimuli, but only modest increases in wide dynamic range (WDR) neurons to mechanical stimuli. Spinal administration of PGE2 produced a bi-directional, dose–response effect on thermally-evoked responses of both WDR and NS neurons when prostaglandin-induced changes in background discharges were controlled for. Thermally evoked responses of WDR and NS neurons were decreased at lesser doses of PGE2, but this trend reversed with greater doses, such that responses of WDR neurons were significantly increased at the greatest dose tested at some test temperatures. PGF2α generally produced non-significant increases in thermally evoked neuronal responses, and this trend occurred primarily in WDR neurons. Both PGE2 and PGF2α produced increases in background discharges of WDR and NS neurons, although this effect was most consistently observed with WDR neurons and PGE2. These behavioral and electrophysiological data suggest that mechanical hyperalgesia induced by spinal administration of PGE2 and PGF2α is mediated mainly by changes in NS neurons. The weak thermal hyperalgesia may reflect changes in WDR neurons.