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Journal of Neuroscience, Vol 4, 2477-2488, Copyright © 1984 by Society for Neuroscience
Decrease of gap junction permeability induced by dopamine and cyclic adenosine 3':5'-monophosphate in horizontal cells of turtle retina
M Piccolino, J Neyton and HM Gerschenfeld
The axon terminals of the H1 horizontal cells of the turtle retina are
electrically coupled by extensive gap junctions. Dopamine (10 nM to 10
microM) induces a narrowing of the receptive field profile of the H1
horizontal cell axon terminals, increases the coupling resistance between
them, and decreases the diffusion of the dye Lucifer Yellow in the network
formed by the coupled axon terminals. These actions of dopamine involve the
activation of D1 receptors located on the membrane of the H1 horizontal
cell axon terminals proper. Increases of the intracellular cyclic AMP
concentration induced by either stimulating the adenylate cyclase activity
with forskolin or inhibiting the phosphodiesterase activity with
isobutylmethylxanthine, theophylline, aminophylline, or compound RO 20-1724
elicit effects similar to those of dopamine on the receptive field profile
of the H1 horizontal cell axon terminals, on their coupling resistance, and
on the diffusion of Lucifer Yellow in the axon terminal network. It is
concluded that dopamine decreases the permeability of the gap junctions
between the axon terminals of the H1 horizontal cells of the turtle retina
and that this action probably involves cyclic AMP as a second messenger.
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