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Title: Oxytocin neurone adaptations to opioids
Author: Munro, Gordon
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1994
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Systemic administration of sulphated cholecystokinin octapeptide (CCK8S) activates central noradrenergic pathways (including possibly the A6 cell group of the locus coeruleus which projects to the SON) and this stimulus to oxytocin secretion into the blood measured by radioimmunoassay was dose-dependently inhibited by the α2-adrenergic agonist clonidine and by morphine; α2- and μ-receptor mediated effects may converge on the same post-receptor mechanism. Cells of the locus coeruleus also show tolerance and dependence to opioids. Withdrawal hypersecretion of oxytocin was significantly attenuated by clonidine, possibly by pre-synaptically blocking the noradrenergic input from the A6 cell group although activation of this pathway by CCK8S alone did not initiate withdrawal. Thus withdrawal excitation of supraoptic oxytocin neurones may involve an excitatory noradrenergic input from the A6 cell group which may become more active during dependence. Tolerance to opioids on excitatory inputs to the SON and within the SON itself may increase the expression of several components excitatory to oxytocin neurones such as endogenous CCK function. An amplification in release of noradrenaline within the SON after removal of central morphine inhibition by naloxone, may then excite oxytocin neurones directly by increasing a voltage dependent Ca2+ conductance. Co-release of oxytocin and CCK would feed back onto the oxytocin neurones and sustain the withdrawal process, whilst the increase in synaptic drive from the A6 cell group and locally within the SON would continue until release of oxytocin and CCK or a pool of readily available Ca2+ had become depleted thereby bringing the withdrawal process to an end.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available