Spinal Opioid Receptors Research Articles

Spinal opioid receptors and inhibition of urinary bladder motility in vivo

The effects of intrathecal injections of morphine and other opioid receptor selective drugs were tested on urinary bladder contractions in the anesthetized rat. Morphine produced dose-related inhibition of bladder motility which was abolished by naloxone. This action was also observed with mu- and delta-opioid receptor agonists but not with a kappa-opioid receptor agonist. These observations appear related to the urinary retention seen clinically with epidural administrations of morphine and support the hypothesis that urinary bladder activity is influenced by spinal opioid mechanisms involving mu- and delta-opioid receptors.

SPINAL SITE OF ANTIARRHYTHMIC ACTION OF MORPHINE AND PETHIDINE IN NORMAL AND SPINAL CORD TRANSECTED DOGS

In coronary artery ligated conscious dogs, intravenous (i.v.) injection of both morphine (8.0 mg/kg) and pethidine (12.0 and 24.0 mg/kg) inhibited the cardiac arrhythmia while naloxone (1.0 mg/kg) facilitated it. Intravenous pretreatment with naloxone completely blocked the morphine induced inhibition of the arrhythmia. Pethidine, however, elicited significant inhibition of the arrhythmia in the naloxone pretreated animals but its duration of action was markedly reduced. The temporal effect of i.v. injection of xylocaine (24.0 mg/kg) was parallel to that of pethidine (24.0 mg/kg) injected i.v. in the naloxone pretreated animals. In cervical spinal cord transected and bilaterally vagotomized dogs, i.v. injection of only 50.0 micrograms/kg of morphine elicited significant inhibition of the arrhythmia which was completely blocked by intrathecal pretreatment with a small dose (1.0 micrograms/kg) of naloxone. The same dose of naloxone, when given intravenously, failed to block the effect of morphine. The antiarrhythmic activity of morphine against the cardiac arrhythmia induced by coronary artery ligation appears to be due to activation of spinal opioid receptors. The local anaesthetic activity of pethidine contributes towards its early phase of antiarrhythmic activity.

Opioid binding sites in the spinal cord

The involvement of spinal opioid receptors and spinal monoaminergic systems, in the antinociceptive effect of intrathecal (IT) salmon calcitonin, has been evaluated by means of the hot plate test, in the rat. Intrathecal pretreatment with 40 μg MR 1452 and 40 μg ICI 154,129, purported selective antagonists respectively for κ and δ opioid receptors did not modify sCT-induced antinociception (2 μg IT). A delay in the development of IT sCT-induced antinociception was observed in rats selectively depleted of cord serotonin (25 mg/kg IP desipramine plus 100 μg IT 5,7-dihydroxytryptamine), whereas the administration of serotonergic antagonists, methysergide and ketanserin, 30 μg IT, did not influence sCT effect. Cord catecholamine depletion (6-OHDA pretreatment) reduced significantly sCT antinociception. A similar reduction was produced by the dopaminergic antagonist haloperidol (15 μg IT), but not by the α-blocker phentolamine (15 μg IT). Findings of this study rule out an involvement of opioid peptidergic system in sCT-induced increase of hot plate latencies at spinal level; a possible involvement of cord dopaminergic receptors is suggested.