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Vol. 54, Issue 4, 655-662, October 1998
/Gs
Stimulation of Adenylyl Cyclase: Relevance to Opioid Tolerance
Department of Biochemistry, State University of New York, Health
Science Center at Brooklyn, Brooklyn, New York 11203 (S.C., M.R.,
A.R.G.), and
Department of Pharmacological and Physiological Sciences,
University of Chicago, Chicago, Illinois 60637 (S.-Z.Y., W.-J.T.)
In the current study, we investigated the neurochemical basis for the
previously reported predominance of stimulatory µ-opioid signaling in
guinea pig longitudinal muscle/myenteric plexus (LMMP) preparations
after chronic in vivo morphine exposure. As expected, recombinant Gs
(rGs) dose-dependently
stimulated adenylyl cyclase (AC) activity in LMMP membranes obtained
from opioid naive as well as tolerant LMMP tissue. However, the
magnitude of the increase was significantly greater in the latter than
in the former. The G
blocking peptide QEHA (50 µM) essentially abolished stimulation by
rGs in LMMP membranes obtained from both opioid naive
and tolerant animals. Interestingly, after partial blockade by lower
QEHA concentrations, the incremental AC stimulation by rGs in tolerant LMMP membranes was no longer observed,
indicating augmented G stimulatory responsiveness.
Concomitant changes in the content of AC isoform protein are consistent
with these biochemical observations. After chronic systemic morphine, AC protein is augmented significantly (56%). This increment is most
likely to be composed of AC isoforms that are stimulated by
G. This is the first demonstration in a complex
mammalian tissue that persistent activation of opioid receptors results in augmented G/Gs AC stimulatory
interactiveness. The relevance of such changes to the manifestation of
opioid tolerance is discussed.
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