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1 Comparative Biosciences, University of Wisconsin, Madison, Wisconsin, United States
2 Madison, Wisconsin, United States; Comparative Biosciences, University of Wisconsin, Madison, Wisconsin, United States
* To whom correspondence should be addressed. E-mail: johnsons{at}svm.vetmed.wisc.edu.
For ectothermic vertebrates, such as reptiles, the effects of opioid receptor subtype activation on breathing are poorly understood. Based on previous studies on mammals and lampreys, we hypothesized that mu (MOR) and delta (DOR) receptor activation would cause respiratory depression while kappa opioid (KOR) receptor activation would have no effect. To address this question, respiration was measured in awake, freely-swimming adult red-eared slider turtles (Trachemys scripta) before and after injection with agonists for specific opioid receptors. DAMGO injections (MOR agonist; 1.5 or 6.5 mg/kg) decreased ventilation (VE) by 72 ± 9% and 95 ± 3%, respectively, at 4.0 h post-injection due to decreased breath frequency and no change in tidal volume (VT). DOR agonists, such as DPDPE (5.0 mg/kg) or DADLE (6.3 mg/kg), decreased VE by 44 ± 10% and 89 ± 4%, respectively, at 4.0 h post-injection due to decreased breath frequency and no change in VT. DADLE also increased breath duration by a maximum of 25 ± 9% at 6.0 h post-injection. U-50488 (KOR agonist; 6.2 mg/kg) increased VT by a maximum of 52 ± 30% at 5.0 h post-injection with variable nonsignificant changes in VE and breath frequency. Naloxone injections (0.25-0.5 mg/kg) given 1.0 h prior to opioid agonist injections blocked all DAMGO-dependent effects, DPDPE-dependent frequency depression, and DADLE-dependent breath duration augmentation for 2.0 h after agonist injections. These results show that MOR and DOR receptor activation causes respiratory depression via decreased breath frequency while VT is increased following KOR receptor activation.
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