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Vol. 54, Issue 2, 419-426, August 1998
Department of Neurobiology, The Weizmann Institute of Science,
76100 Rehovot, Israel (I.N., T.A.-R., R.L., M.B., Z.V.), and
The Israel
Institute for Biological Research, 74100 Ness Ziona, Israel
(E.H.)
Adenylyl cyclase superactivation, a phenomenon by which chronic
activation of inhibitory Gi/o-coupled receptors leads to an increase in cAMP accumulation, is believed to play an important role as
a compensatory response of the cAMP signaling system in the cell.
However, to date, the mechanism by which adenylyl cyclase activity is
regulated by chronic exposure to inhibitory agonists and the nature of
the adenylyl cyclase isozymes participating in this process remain
largely unknown. Here we show, using COS-7 cells transfected with the
various AC isozymes, that acute activation of the D2
dopaminergic and m4 muscarinic receptors inhibited the activity of
adenylyl cyclase isozymes I, V, VI, and VIII, whereas types II, IV, and
VII were stimulated and type III was not affected. Conversely, chronic
receptor activation led to superactivation of adenylyl cyclase types I,
V, VI, and VIII and to a reduction in the activities of types II, IV,
and VII. The activity of AC-III also was reduced. This pattern of
inhibition/stimulation of the various adenylyl cyclase isozymes is
similar to that we recently observed on acute and chronic activation of
the µ-opioid receptor, suggesting that isozyme-specific adenylyl
cyclase superactivation may represent a general means of cellular
adaptation to the activation of inhibitory receptors and that the
presence/absence and intensity of the adenylyl cyclase response in
different brain areas (or cell types) could be explained by the
expression of different adenylyl cyclase isozyme types in these areas.
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