Data from: Light-sensitive Ca2+ signaling in the mammalian choroid

The choroid is the thin, vasculature-filled layer of the eye situated
between the sclera and the retina, where it serves the metabolic needs of
the light-sensing photoreceptors in the retina. Illumination of the
interior surface of the back of the eye (fundus) is a critical regulator
of subretinal fluid homeostasis, which determines the overall shape of the
eye, but it is also important for choroidal perfusion. Noted for having
some of the highest blood flow rates in the body, the choroidal
vasculature has been reported to lack intrinsic, intravascular
pressure-induced (myogenic) autoregulatory mechanisms. Here, we ask how
light directly regulates choroid perfusion and ocular fluid homeostasis,
testing the hypothesis that light facilitates ocular fluid absorption by
directly increasing choroid endothelial permeability and decreasing
choroid perfusion. Utilizing ex vivo pressurized whole-choroid and
whole-eye preparations from mice expressing cell-specific Ca2+ indicators,
we found that the choroidal vasculature has two intrinsically
light-sensitive Ca2+-signaling mechanisms: one increases Ca2+-dependent
production of nitric oxide in choroidal endothelial cells, the other
promotes vasoconstriction through Ca2+ elevation in vascular smooth muscle
cells. In addition, we found that choroidal flow, or pressure, modulates
endothelial and smooth muscle photosensitivity and trans-retinal
absorption of fluid into the choroid. These results collectively suggest
that the choroid vasculature exhibits an inverted form of autoregulatory
control, where pressure- and light-induced mechanisms work in opposition
to regulate blood flow and maintain fluid balance in response to changes
in light and dark, aligning with the metabolic needs of photoreceptors.