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Query: UMLS:C0344307 (
analgesia
)
28,200
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
It is well admitted that stress induces
analgesia
(SIA) via endogenous opioid release. However, there is evidence that stressful events play a role in the pathogenesis of pain, but little is known about mechanisms underlying such pain vulnerability. Previous studies reported that a single opioid exposure activates NMDA-dependent pronociceptive systems leading to long-term pain vulnerability after
analgesia
. Here, we studied whether prior inflammatory pain or/and opioid experiences may favour the development of pain vulnerability after non-nociceptive environmental stress (NNES). Nociceptive threshold (NT) changes were evaluated by paw pressure vocalization test. By contrast to discrete SIA observed in naive rats, 1 h stress induced hyperalgesia (SIH) for several hours (15-65% NT decrease) in pain and opioid experienced rats. Repetition of NNES induced an 18- to 22-fold SIH enhancement (3-4 days), whereas SIA decreased. SIH was still observed 4 months after pain and opioid experiences. This phenomenon is referred to as latent pain sensitization. Furthermore, a fentanyl ultra-low dose (
ULD
, 50 ng/kg) administration, mimicking SIA in naive rats, induced hyperalgesia (65% NT decrease, 4 h), not
analgesia
, in pain and opioid-experienced rats. This indicates that low levels of opioids induce opposite effects, that is
analgesia
vs hyperalgesia dependent on prior life events. In pain and opioid-experienced rats, NMDA receptor antagonists, ketamine or BN2572, completely prevented hyperalgesia when injected just before NNES or fentanyl
ULD
. This latent pain sensitization model may be important for studying the transition from acute to chronic pain and individual differences in pain vulnerability associated with prior life events.
...
PMID:Non-nociceptive environmental stress induces hyperalgesia, not analgesia, in pain and opioid-experienced rats. 1729 8