Choroidal innervation in primate eyes

Abstract

Arteries and arterioles of the choroid are surrounded by numerous nerve fibers staining for nitric oxide synthase (NOS) and vasoactive intestinal peptide (VIP). In most mammalian eyes these nerve fibers derive from the pterygopalatine ganglion via the facial nerve. Stimulation of the facial nerve causes vasodilation of the choroidal vasculature. In primates with a well developed fovea centralis there are ganglion cells in the choroidal stroma which in human eyes amount to around 2000. The postganglionic nerve fibers of these choroidal ganglion cells (CGC) join the perivascular nerve fiber plexus. The CGC stain for NOS and VIP like the nerve cells within the pterygopalatine ganglion. There are, however, differences between the two cell populations. Immunohistochemical and ultrastructural classification of the CGC show that in addition to NOS and VIP almost half of the cells stain for calretinin, single ones for neuropeptide Y (NPY) and galanin. A number of cells is in close contact with numerous boutons staining for nNOS, VIP, NPY, tyrosine hydroxylase (TH), vesicular monoaminergic transporter (VMAT)2, vesicular acetylcholine transporter (VACHT), calretinin, and NPY. These data indicate a more complex integrative function of CGCs e.g. volume regulation in parallel with ciliary muscle contraction during accommodation. Ultrastructural and immunohistochemical studies indicate, that CGCs in addition may have mechanosensory properties. Whether they are involved in volume-regulatory functions independent of accommodation is not yet known. In glaucoma disease the number of CGCs is significantly reduced. This holds true for eyes with primary open angle glaucoma, pseudoexfoliation glaucoma and experimentally induced monkey glaucoma indicating that elevated IOP is involved in the pathogenesis of glaucomatous CGC-degeneration.