Multiple opioid system involvement in the mediation of parasitic-infection induced analgesia

Abstract

Although parasite modification of host behaviour is well established, little is known about the mechanisms underlying such effects. The present study examined the relationships between subclinical infection with the enteric sporozon parasite, Eimeria vermiformis, nociceptive responses and endogenous opioid systems in male mice. Infected mice displayed significant analgesia which increased through the prepatent period [oocyst formation (pre-infective); days 1–7 post-infection (PI)], reached a maximum with the onset of patency (onset oocyst shedding and infectivity; days 7–8 PI) and declined during patency (oocyst shedding), with response latencies declining to basal levels with the cessation of oocyst production and infectivity (day 15 PI). The increasing nociception during the prepatent period (day 4 PI) was associated with k opioid mechanisms, being reduced by the k antagonist, nor-binaltorphimine, and insensitive to either the σ antagonist, ICI 174,864, or the general, predominately μ antagonist, naloxone. Maximum analgesia (day 7 PI) associated with the onset of patency (infectivity) was sensitive to both the k and μ antagonists, but insensitive to the σ antagonist, while the declining analgesia during patency (day 10 PI) was reduced by the μ and σ antagonists, but was insensitive to the k antagonist. These results indicate that μ, σ and k opioid systems are involved in the mediation of su subclinical parasitic infection-induced analgesia and likely other associated parasite-induced modifications of host behaviour.