EXTREME RESPONSIVENESS OF THE PUPIL OF THE DARK-ADAPTED MOUSE TO STEADY RETINAL ILLUMINATION

PURPOSE. TO measure the dependence of the size of the pupils of mice o n steady retinal illumination. METHODs. Anesthetized C57BL/6 mice aged 7 to 8 weeks were placed in a ganzfeld chamber in darkness, and in mo nochromatic (510 nm) and white light whose intensity was varied more t han 6 log units. The pupils of the mice were photographed with an infr ared video camera and recorded on videotape and the pupil areas determ ined by digital image analysis of the video recordings. RESULTS. Fully dark-adapted murine pupils had an area of 2.29 +/- 0.35 mm(2). The mi nimum pupil size at saturating intensity was 0.10 +/- 0.05 mm(2). The steady state pupil area declined to half its dark-adapted maximum when ganzfeld luminance was 10(-5) scotopic candela (scot. ed) per meter s quared. Pupil area declined to 20% of the dark-adapted magnitude at ap proximately 10(-3) scot. cd/m(2). CONCLUSIONS. The mouse pupil can reg ulate retinal illumination by a factor exceeding 20. The neural circui try that determines steady state murine pupil size is extremely sensit ive to retinal illumination and under these experimental conditions is controlled almost exclusively by rod signals. This follows, because t he ganzfeld illuminance (10(-5) scot, cd/m(2)) that causes the pupil t o constrict to half its dark-adapted value corresponds to only approxi mately 0.01 photoisomerization per rod per second, whereas 80% reducti on in pupil area occurs at approximately 1 photoisomerization per rod per sec. Based on this extreme responsiveness to steady illumination, the hypothesis is proposed that the murine pupil functions to protect a retinal circuit that can become saturated at extremely low photon ca pture rates. General principles of dark-adapted retinal circuitry supp ort the identification of the first three neurons in the circuit as th e rod, the rod bipolar, and the AII-amacrine. The rod and rod bipolar neurons do not approach saturation at the intensities at which the pup il constricts, however, and it seems unlikely that the AII-amacrine do es. Thus the retinal neurons protected from saturation by the mouse pu pil constrictions are probably ganglion cells with large receptive fie lds that have sustained responses.