Background: Recently we found that fever (part of HIV-related wasting) is induced by the action of the human immunodeficiency virus-1 (HIV-1) envelope glycoprotein (gp120) in the preoptic anterior hypothalamus (POAH). As the opioid system plays a role in the pathogenesis of HIV-1, in the present study we sought to examine the capacity of the opioid system to regulate the febrile response induced by gp120.
Methods: Stainless steel cannulas were stereotactically into the POAH, and a biotelemetry system was used to monitor the body temperature (Tb changes). We examined the in vivo effects of naloxone as well as highly opioid-selective receptor antagonists, on gp120-induced fever.
Results: Pretreatment with naloxone or the mu-opioid receptor-selective antagonist, cyclic d-Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH(2) (CTAP), significantly delayed the febrile response induced by gp120. In contrast, naltriben (NTB), a selective antagonist for the delta-2 opioid receptor, did not cause any effect on gp120-induced fever.
Conclusion: These results (1) provide pharmacologic evidence of a functional in vivo interaction between the opioid system and this viral protein in the POAH and (2) show that mu-opioid receptors can regulate gp120-induced fever.
Keywords: Fever; HIV; Opioid system and gp120.
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