The Journal of Cell Biology, Vol 95, 445-452, Copyright © 1982 by The Rockefeller University Press
Elevation of cyclic AMP activates an actin-dependent contraction in teleost retinal rods
P O'Connor and B Burnside
Agents which elevate cyclic AMP (cAMP) cause teleost retinal rods to
contract. We have characterized this cAMP effect and have evaluated the
role of the cytoskeleton in cyclic nucleotide-induced contraction, using
actin and microtubule inhibitors. The necklike myoid region of the rod
contracts in the dark and elongates in the light. If long, light-adapted
rods are cultured with cAMP analogs and IBMX, rods contract to their short
dark-adapted position. Cyclic nucleotide- induced rod contraction occurs in
constant light, requires a phosphodiesterase inhibitor, and is specific to
cAMP (db cyclic GMP, 8- bromocyclic GMP, 5'AMP, and adenosine have no
effect on rod myoid length). Cyclic AMP effects on rod length are
consistent with observations from several species that cAMP levels are
higher in dark- adapted than in light-adapted retinas. Since rod myoids
contain paraxially aligned actin filaments and microtubules, we have used
the motility inhibitors cytochalasin D and cold and nocodazole to
investigate the roles of these cytoskeletal elements in rod contraction.
Cyclic nucleotide-induced contraction is not inhibited when myoid
microtubules are disrupted with cold and nocodazole treatments, but
contraction is blocked if myoid actin filaments are disrupted with
cytochalasin D. Thus, we conclude that actin filaments, but not
microtubules, are required for rod contraction. We propose that rod
contraction in vivo is triggered by a rise of cytoplasmic cAMP at onset of
darkness and that this contraction is mediated by an actin- dependent
mechanism.
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