Premium
Aromatic L‐Amino Acid Decarboxylase Is Modulated by D1 Dopamine Receptors in Rat Retina
Author(s) -
Rossetti Zvani L.,
Silvia Christopher P.,
Krajnc Dimitrij,
Neff Norton H.,
Hadjiconstantinou Maria
Publication year - 1990
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 - 10.1111/j.1471-4159.1990.tb02320.x
Subject(s) - dopamine , aromatic l amino acid decarboxylase , dopamine receptor , retina , receptor , chemistry , dopamine receptor d1 , neuroscience , biochemistry , pharmacology , endocrinology , medicine , microbiology and biotechnology , biology
Aromatic L‐amino acid decarboxylase (AAAD) activity of rat retina increases when animals are placed in a lighted environment from the dark. The increase of activity can be inhibited by administering the selective dopamine D1 receptor agonist SKF 38393, but not the selective D2 agonist quinpirole, or apomorphine. Conversely, in the dark, enzyme activity can be enhanced by administering the selective D1 antagonist SCH 23390 or haloperidol, but not the selective D2 antagonist (–)‐sulpiride. Furthermore, in animals exposed to room light for 3 h, the D1 agonist SKF 38393 reduced retinal AAAD activity, and this effect was prevented by prior administration of SCH 23390. In contrast, quinpirole had little or no effect when administered to animals in the light. Kinetic analysis indicated that the apparent V max for the enzyme increases with little change in the apparent K m for the substrate 3,4‐dihydroxyphenylalanine or the cofactor pyridoxal‐5′‐phosphate. We suggest that dopamine released in the dark tonically occupies D1 receptors and suppresses AAAD activity. When the room light is turned on, D1 receptors are vacated and selective D1 agonists can either prevent the rise of AAAD or reverse light‐enhanced AAAD activity.