The selective δ-opioid receptor agonist deltorphin II (25.0-100.0 μg, i.c.v.) produced biphasic effects on core temperature in rats, in which hypothermia was followed by hyperthermia. Pretreatment with the selective δ-opioid receptor antagonist, naltrindole (25.0 μg, i.c.v.), blocked hypothermia produced by deltorphin II and had a tendency to potentiate the hyperthermic effect of deltorphin II. The non-selective opioid receptor antagonist naloxone (1.5 mg kg-1, s.c.) potentiated hypothermia, and blocked hyperthermia, produced by deltorphin II (100.0 μg). Also, naloxone potentiated hypothermia produced by a lower dose of deltorphin II (25.0 μg), which did not produce hyperthermia. A similar pattern was found for the selective μ-opioid receptor antagonist, β-funaltrexamine (5.0 μg, i.c.v.), which potentiated and blocked deltorphin II-induced hypo- and hyperthermia, respectively. The selective κ-opioid receptor antagonist nor-binaltorphimine (20.0 μg, i.c.v.) had no effects on deltorphin II-induced temperature changes. The present results suggest that deltorphin II produces hypothermia through activation of δ-opioid receptors, whereas the hyperthermic effect of deltorphin II involves activation of μ-opioid receptors. This μ-opioid receptor stimulatory effect of deltorphin II is furthermore more pronounced than was anticipated based on the reported in vitro properties of this compound. The biphasic effect of deltorphin II implies a negative interaction between δ- and μ-opioid receptors in thermoregulation in rats.
- Body temperature
- Deltorphin II
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience