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Vol. 281, Issue 1, 109-114, 1997
-glucuronide Antinociception1
The Cotzias Laboratory of Neuro-Oncology, Memorial Sloan-Kettering
Cancer Center, New York, New York (G.C.R., L.L., Y.-X.P., W.S.,
G.W.P.); Departments of
Neurology & Neuroscience and Pharmacology,
Cornell University Medical College, New York, New York (G.W.P.);
Neuropsychology Doctoral Sub Program, City University of New York, New
York, New York (L.L., J.C., R.J.B.); and
Department of Psychology,
Queens College, City University of New York, Flushing, New York
(R.J.B.)
In an effort to correlate the recently cloned MOR-1 receptor with the
pharmacological actions of morphine and morphine-6
-glucuronide (M6G), we have used an antisense paradigm. Rats were injected intracerebroventricularly (i.c.v.) with antisense oligodeoxynucleotides on days 1, 3 and 5 and tested for analgesia on day 6 after
administration of morphine or M6G i.c.v. or after microinjection of
morphine directly into either the periaqueductal gray or the locus
coeruleus. When given i.c.v., the antisense oligodeoxynucleotide
targeting the 5
-untranslated region of exon 1 significantly decreased
the analgesic actions of morphine administered i.c.v. or microinjected directly into the periaqueductal gray or locus coeruleus, with the most
profound inhibition occurring in the periaqueductal gray. Thus,
antisense oligodeoxynucleotides administered into the lateral ventricle
can diffuse into the brainstem and interfere with morphine actions. A
mismatch antisense oligodeoxynucleotide with the same base composition
in which the sequence of four bases was changed was inactive. This same
exon 1 antisense oligodeoxynucleotide, which was active against
morphine analgesia, failed to block M6G analgesia. In contrast,
antisense sequences from exons 2 and 3 decreased M6G, and not morphine,
analgesia. The antisense oligodeoxynucleotide against exon 4 slightly
decreased both morphine and M6G antinociception. These results confirm
the antisense mapping studies on exons 1, 2 and 3 of MOR-1 in mice,
which implied the presence of a novel µ receptor subtype responsible
for M6G analgesia that may represent a splice variant of MOR-1. Unlike
in mice, the probe against exon 4 had a small effect on M6G analgesia.
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