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1 Department of Physiology, University of Wisconsin School of Medicine, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: pmlalley{at}facstaff.wisc.edu.
µ-Opioid receptor agonists depress tidal volume, decrease chest wall compliance and increase upper airway resistance. In this study, potential neuronal sites and mechanisms responsible for the disturbances were investigated, dose-response relationships were established and it was determined whether general anaesthesia plays a role. Effects ofµ-opioid agonists on membrane properties and discharges of respiratory bulbospinal, vagal and propriobulbar neurons and phrenic nerve activity were measured in pentobarbital-anaesthetized and unanaesthetized decerebrate cats. In all types of respiratory neurons tested, threshold i.v. doses of the µ-opioid agonist fentanyl slowed discharge frequency and prolonged duration without altering peak discharge intensity. Larger doses postsynaptically depressed discharges of inspiratory bulbospinal and inspiratory propriobulbar neurons that might account for depression of tidal volume. Iontophoresis of the µ-opioid agonist DAMGO also depressed the intensity of inspiratory bulbospinal neuron discharges. Fentanyl given i.v. prolonged discharges leading to tonic firing of bulbospinal expiratory neurons in association with reduced hyperpolarizing synaptic drive potentials, perhaps explaining decreased inspiratory phase chest wall compliance. Lowest effective doses of fentanyl had similar effects on vagal Post-Inspiratory (laryngeal adductor) rnotoneurons whereas in vagal laryngeal abductor and pharyngeal constrictor motoneurons, depression of depolarizing synaptic drive potentials led to sparse, very low frequency discharges. Such effects on three types of vagal motoneurons might explain tonic vocal fold closure and pharyngeal obstruction of airflow. Measurements of membrane potential and input resistance suggest the effects on bulbospinal Aug-E neurons and vagal motoneurons are mediated presynaptically. Opioid effects on the respiratory neurons were similar in anesthetized and decerebrate preparations.
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