Abstract：
:Recent evidence has suggested that cholecystokinin (CCK) may act as a physiological opiate antagonist. Both the overlap of CCK and opiate systems within the central nervous system and the fact that exogenous CCK can antagonize opiate analgesia suggest that endogenous CCK systems interact with opiate-mediated pain inhibitory systems. In the present series of experiments, we examined the effect of the CCK receptor antagonist proglumide on various forms of morphine analgesia. We have observed that proglumide can potentiate morphine analgesia following systemic, intrathecal or intracerebral administration of these drugs. Endogenous CCK systems do not appear to be tonically active since neither systemic, intrathecal nor intracerebral proglumide typically produced measurable analgesia in the absence of morphine. These data suggest that CCK may be released in response to opiate administration and acts to return the organism toward its basal level of pain sensitivity. If such a hypothesis is in fact true, then CCK blockade may be of clinical value in the treatment of pain.
journal_name
Brain Resjournal_title
Brain researchauthors
Watkins LR,Kinscheck IB,Mayer DJdoi
10.1016/0006-8993(85)91511-2subject
Has Abstractpub_date
1985-02-18 00:00:00pages
169-80issue
1-2eissn
0006-8993issn
1872-6240pii
0006-8993(85)91511-2journal_volume
327pub_type
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