Regulation of tryptophan hydroxylase expression by a retinal circadian oscillator in vitro. Brain Res 1995 Apr 24;677(2):283-90
Date
04/24/1995Pubmed ID
7552254DOI
10.1016/0006-8993(95)00166-nScopus ID
2-s2.0-0028931204 (requires institutional sign-in at Scopus site) 48 CitationsAbstract
Many aspects of retinal physiology are controlled by a circadian clock including at least two steps in the melatonin synthetic pathway: the activity of the enzyme, N-acetyltransferase (NAT), and mRNA levels of the rate-limiting enzyme trytophan hydroxylase (TPH). Light and dopamine (through D2-like dopamine receptors) can phase shift the clock, and can also acutely inhibit NAT activity, resulting in supressed melatonin synthesis. In this paper, we show that eyecups cultured in constant darkness maintain a clock-controlled rhythm in TPH mRNA, with low levels in early day, rising to a peak in early night. Both eyecups and isolated retinas, cultured in light during the day, also exhibit a similar increase in TPH mRNA levels, indicating that this expression is not acutely inhibited by light. Treatment with light or quinpirole (D2 dopamine receptor agonist) in early night, at a time and dose that acutely inhibits NAT activity, does not change levels of TPH mRNA. Addition of eticlopride (D2 dopamine receptor antagonist) during the day, also has no effect on the normal daytime increase in TPH message levels. Therefore, TPH mRNA level is controlled by a circadian clock located within the eye, but acute effects of light or dopamine are not detected.
Author List
Green CB, Cahill GM, Besharse JCAuthor
Joseph C. Besharse PhD, MA Emeritus Professor in the Cell Biology Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCells, Cultured
Circadian Rhythm
Dopamine Agonists
Dopamine Antagonists
Ergolines
Gene Expression Regulation
Photoperiod
Quinpirole
RNA, Messenger
Retina
Salicylamides
Tryptophan Hydroxylase
Xenopus laevis
