Abstract: |
The recent cloning of mu, delta and kappa1, opioid receptors has provided opportunities in the study of their pharmacology. Using an antisense strategy developed against delta and kappa1 opioid receptors, we designed an antisense oligodeoxynucleotide directed against the 5′-untranslated region of MOR-1 clone, 51-70 bp upstream from the initiating ATG. Microinjection of this antisense oligodeoxynucleotide directly into the periaqueductal gray on Days 1, 3 and 5 completely blocked the analgesic actions of morphine administered into the periaqueductal gray on Day 6 (p < 0.001), 24 hr after the last antisense treatment. Rats treated with vehicle or with a mismatch oligodeoxynucleotide in which two pairs of bases from the antisense sequence had been switched were not significantly affected. These findings confirm the pharmacological relevance of the MOR-1 clone and its involvement in morphine's actions. © 1994. |
Keywords: |
controlled study; nonhuman; comparative study; animal; animal tissue; animal experiment; histology; molecular cloning; drug antagonism; molecular sequence data; rat; base sequence; rats; rats, sprague-dawley; morphine; analgesia; mu opiate receptor; receptors, opioid, mu; tail flick test; microinjections; oligonucleotides, antisense; dose time effect relation; receptor subtype; mu opioid receptor; antisense oligodeoxynucleotide; periaqueductal gray matter; periaqueductal gray; male; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; mor-1 clone; intracerebral drug administration; antisense treatment
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