期刊
PAIN
卷 97, 期 1-2, 页码 33-45出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/S0304-3959(01)00487-0
关键词
prostaglandin E-2; prostaglandin F-2 alpha; hyperalgesia; spinal neurons
资金
- NINDS NIH HHS [NS 35794] Funding Source: Medline
The effects of intrathecal (i.t.) administration of prostaglandin E-2 (PGE(2)) and prostaglandin F-2alpha (PGF(2alpha)) on behavioral and spinal neuronal responses to mechanical and thermal stimuli were examined in rats. i.t. Administration of either PGE(2) (1-100 nmol) or PGF(2alpha) (1-100 nmol) produced a robust, dose-dependent mechanical hyperalgesia, but only a weak thermal hyperalgesia and touch-evoked allodynia. Spinal administration of either PGE(2) (100 pmol-100 mnol) or PGF(2alpha) (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 PGE(2) 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 PGE(2), 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. PGF(2alpha) generally produced non-significant increases in thermally evoked neuronal responses, and this trend occurred primarily in WDR neurons. Both PGE(2) and PGF(2alpha) produced increases in background discharges of WDR and NS neurons, although this effect was most consistently observed with WDR neurons and PGE(2). These behavioral and electrophysiological data suggest that mechanical hyperalgesia induced by spinal administration of PGF(2) and PGF(2alpha) is mediated mainly by changes in NS neurons. The weak thermal hyperalgesia may reflect changes in WDR neurons. (C) 2002 International Association for the study of Pain. Published by Elsevier Science B.V. All rights reserved.
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