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pubmed:abstractText |
The present study examined the nociceptive responses (50 degrees C, hot-plate) of uninfected and subclinically parasitized male mice exposed to the odor of a predator, an ecologically relevant threatening stimulus. In uninfected mice a 15-min exposure to 2-propylthietane, the major component of weasel odor, induced a naloxone-reversible opioid analgesia. A 30-s exposure elicited a shorter duration and lower amplitude 'non-opioid' analgesia that was insensitive to naloxone, partially sensitive to either the serotonin-1A (5-HT1A) agonist, 8-OH-DPAT, or the GABAA antagonist, bicuculline, and blocked by the competitive N-methyl-D-aspartate (NMDA) antagonist, NPC 12626. In contrast, mice chronically (25 days) and subclinically infected with the murine nematode, Heligmosomoides polygyrus, failed to show a significant non-opioid analgesia and displayed a markedly lower level of opioid analgesia than uninfected mice. These results suggest that NMDA receptor mechanisms are potently associated with the expression of the analgesia arising from exposure to the naturally aversive stimulus of predator odor. These findings also demonstrate that parasites, and likely other subchronic infections, can have a significant impact on the display of opioid and non-opioid stress-induced analgesia arising from exposure to the ethologically relevant stimulus of predator odor.
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