Abstract
The decrease in nociceptive threshold has been demonstrated in rats exposed to 24 C and cold environment (-3 C) for alternate one hour periods from 10:00-17:00 hours and then kept with cold temperature from 17:00-10:00 hours in the following morning for several days. This model is referred to as the SART (Specific Alternation of Rhythm in Temperature) stress. In the present study, to verify the mechanisms underlying such hyperalgssia, antinociceptive effects of various neuroactive drugs were investigated with the intrathecal injections. The analgesic effects of intrathecal serotonin (5-HT, 30 and 100 nmol/rat), 1-(m-chlorophenyl)-biguanlde hydrochlorlde (mCPBG,10-10Omol/rat, a 5-HT3 agonist) and clonldine (30nmoVrat, an 0~ agonist) in SART stressed rats were significantly greater than in normal rats. (±)-8-hydroxy-2-(di-n-propylamino) tetralin hydrochloride (DPAT, a 5-HT~A agonist) and CGS12066B (a 5-HT,B agonist) produced hyperalgesic action in normal rats. An intrathecal a-methyl 5-HT (a 5-HT2 agonist), phenylephrine (an o¢, agonist), isoproteranol (a I~ agonist) and dopamine had no influence on the nociceptive threshold in both normal and SART stressed rats. On the other hand, the analgesic effects of intrathecal morphine and [D-Ala =, MetS] enkephalinamide (an opioidergic I~ agonist) or [D-Pen~,S]-enkephalin (a ~ agonist) were same degree between SART stressed and normal rats. These results suggest that SART stressed rat exhibit the hyperalgesis resulting from the decreased activltiss of descending monoaminergic pain inhibitory systems, probably mediated by either 5-HT~ serotonergic or o~ noradrenergic receptors in the spinal dorsal horn.
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