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Genetic deletion of mu opioid receptors from Kölliker‐Fuse neurons reduces morphine‐induced respiratory depression

Activation of mu opioid receptors in the pontine Kölliker‐Fuse (KF) causes a reduction in respiratory rate in anesthetized rats. We have previously shown that mu opioid agonists hyperpolarize a population of KF neurons (Levitt et al., J Physiol, 2015). The goal of these experiments was to determine the contribution of the opioid‐sensitive KF neurons to the reduction in respiratory rate caused by systemic administration of the opioid agonist morphine. Targeted deletion of mu opioid receptors was accomplished by viral expression of Cre recombinase in the KF of mice with floxed mu opioid receptors. Experiments were performed 4– 6 weeks later. In whole‐cell recordings from brain slices, infected KF neurons were no longer hyperpolarized by opioid agonist, confirming deletion of mu opioid receptors. Head‐out plethysmography was used to measure respiratory rate. Morphine (10 mg/kg, ip) caused a significantly smaller reduction in respiratory rate in mice with bilateral deletion of mu opioid receptors from KF, compared to uninjected or GFP injected controls. The time‐course for the effect of morphine was also delayed in mice lacking mu receptors in KF neurons. Thus, opioid‐sensitive KF neurons contribute to, but are not entirely responsible for, systemic morphine‐induced respiratory depression.