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Adenosine A 2a receptor‐mediated inhibition of rod opsin mRNA expression in tiger salamander
Author(s) -
Alfinito Peter D.,
Alli Roshni,
TownesAnderson Ellen
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.01162.x
Subject(s) - opsin , adenosine , biology , rhodopsin , adenosine a1 receptor , adenosine kinase , agonist , microbiology and biotechnology , endocrinology , adenosine receptor , adenosine deaminase , medicine , receptor , biochemistry , retinal
The neuromodulator adenosine mediates dark‐adaptive changes in retinal photoreceptors through A 2a receptors. In cold‐blooded vertebrates, opsin mRNA expression is lower at night than during the day. In the present study, we tested whether adenosine could inhibit opsin mRNA expression in cultured rod cells and if endogenous adenosine acts to suppress opsin mRNA in the intact retina at night. Semi‐quantitative in situ hybridization showed that treatment with 100 n m of the A 2a /A 2b agonist N 6 ‐[2‐(3,5‐dimethoxyphenyl)‐2‐(2‐methylphenyl)‐ethyl]adenosine (DPMA) reduced opsin mRNA 41% in cultured rod cells. The effect of DPMA was blocked by 10 µ m of the A 2a antagonist 8‐(3‐chlorostyryl)caffeine (CSC) but not by 10 µ m of the A 2b antagonist alloxazine. One micromolar adenosine alone had no effect on opsin mRNA. However, in the presence of the adenosine deaminase inhibitor erythro ‐9‐(2‐hydroxy‐3‐nonyl)adenine hydrochloride (EHNA), 1 µ m adenosine reduced opsin mRNA 61%. EHNA alone reduced opsin mRNA by 26%. Consistent with an A 2a receptor mechanism, 100 n m forskolin (adenylate cyclase agonist) decreased opsin mRNA 34%. Finally, northern blots showed that intravitreal injection of 10 µ m CSC at night increased opsin I mRNA 38%. Thus, endogenous adenosine suppresses rod opsin I mRNA expression at night; in vitro results indicate this reduction occurs through A 2a ‐like receptor binding and stimulation of adenylate cyclase activity.