Purpose
To make best use of light at different intensities, the retina shifts from high sensitivity/low resolution in dim light, to low sensitivity/high resolution in strong light. Dopamine (DA) and nitric oxide (NO) play important roles in this shift, but the detailed mechanisms are unknown. The optokinetic response (OKR), an inborn visual reflex, is a rapid, noninvasive read-out of inner-retinal function such as contrast sensitivity (CS). Here we tested whether DA and NO mediate light-adaptation of CS in chick retina.
Methods
In daytime we tested the photopic spatial CS of OKR in White Leghorn cockerels, age P5-P12, adapted for ≥60 min to “light” (Imean=1.98 log cd/m2) or “dark” (Imean=-0.72 log cd/m2), using OptoMotry®. If endogenous DA or NO mediates light-adaptation, agonists should mimic light-adaptation in the dark, and antagonists should mimic dark-adaptation in the light. Under isoflurane anesthesia, we injected intravitreally 20µL of vehicle containing: (a) nonspecific DA agonist, ADTN (50mM) to mimic light-adaptation; or (b) D1R antagonist SCH23390 (500µM), (c) D2R antagonist spiperone (200 µM), or (d) NO synthase (NOS) inhibitor L-NIO (5mM), to mimic dark-adaptation.
Results
In light, spatial CS varied with spatial frequency (SF), peaking at intermediate SF (~0.5 cyc/deg) and decreasing at lower and higher SFs (Fig. 1), as does CS in mice (Umino et al., 2008). Dark-adaptation reduced peak CS from 15.0 to 7.5, and shifted best SF from 0.5 to 0.32 cyc/deg, by reducing CS at higher SFs (Fig. 1). This change was reversed by ADTN in the dark (Fig. 1), and dark-adaptation was mimicked in the light by spiperone or L-NIO, but not by SCH23390 (Figs. 2, 3, 4).
Conclusions
Light-adaptation increases DA and NO release in the retina, shifting retinal circuit functions (CS, spatial resolution) to the light-adapted state. DA does this via D2-like, not D1-like receptors. Adaptation of spatiotemporal CS in the chick retina closely resembles that reported for the mouse, making it an excellent model for determining the cellular sites and mechanisms of action of DA and NO in neural adaptation.