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Antisense oligodeoxynucleotides against mu- or kappa-opioid receptors block agonist-induced body temperature changes
X H Chen1, E B Geller, J K de Riel
1Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Abstract:
PL017 and dynorphin A1-17 were shown previously to cause a marked increase and a profound decrease in body temperature (Tb), respectively. In this study, we examined whether an antisense (AS) oligodeoxynucleotide (oligo) against cloned mu or kappa opioid receptors could block PL017- or dynorphin A-induced body temperature changes. Treatment with an AS oligo against mu receptors, but not sense (S) oligo, missense (MS) oligo or artificial cerebrospinal fluid (aCSF), abolished PL017-induced hyperthermia. In addition, treatment with an AS oligo against kappa receptors, but not S oligo, MS oligo or aCSF, greatly attenuated dynorphin A-induced hypothermia. This study further supports the notion that mu and kappa receptors mediate Tb regulation.
Insights
Antisense oligonucleotides targeting mu opioid receptors blocked PL017-induced hyperthermia, while those targeting kappa opioid receptors attenuated dynorphin A-induced hypothermia, confirming receptor roles in body temperature regulation.
Area of Science:
- Neuroscience
- Pharmacology
- Physiology
Background:
- Opioid peptides modulate body temperature (Tb). PL017 increases Tb, while dynorphin A decreases Tb.
- Mu and kappa opioid receptors are implicated in various physiological processes.
Purpose of the Study:
- To investigate the role of mu and kappa opioid receptors in regulating body temperature using antisense oligonucleotides.
- To determine if specific opioid receptor antagonism can block opioid-induced thermoregulatory changes.
Main Methods:
- Administration of antisense (AS) oligodeoxynucleotides (oligos) targeting mu or kappa opioid receptors.
- Assessment of the effects of AS oligos on PL017-induced hyperthermia and dynorphin A-induced hypothermia.
- Control treatments included sense (S) oligos, missense (MS) oligos, and artificial cerebrospinal fluid (aCSF).
Main Results:
- AS oligos against mu receptors abolished PL017-induced hyperthermia.
- AS oligos against kappa receptors significantly attenuated dynorphin A-induced hypothermia.
- Control oligos and aCSF did not affect the observed body temperature changes.
Conclusions:
- Mu opioid receptors mediate PL017-induced increases in body temperature.
- Kappa opioid receptors mediate dynorphin A-induced decreases in body temperature.
- These findings reinforce the critical role of specific opioid receptors in thermoregulation.