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A. Bergua, M. Kapsreiter, A. Brehmer, W.L. Neuhuber, F.E. Kruse, F. Schrödl; Innervation of the Intraoptic Nerve Course of the Human Central Retinal Artery . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3893.
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Purpose: The central retinal artery (CRA) is the main source of retinal nutrition– and oxygen supply. The intraocular branches show auto regulation regarding blood flow while lacking autonomic innervation. Controversy discussed is the innervation of the extra ocular part of this vessel coursing within the optic nerve. Since this initial part is essential for maintaining retinal blood supply, hence also for pathophysiological conditions, aim of this study was to more precisely describe the autonomic innervation of the extra ocular part of the human CRA within the optic nerve. Methods: Meeting the declaration of Helsinki, optic nerves from human donor eyes were processed for cytochemistry and single and double immunohistochemistry of the following markers: calcitonin–gene related peptide (CGRP), substance P (SP), neuronal nitric oxide synthase (nNOS)/NADPH–diaphorase, vasoactive intestinal peptide (VIP), tyrosine hydroxylase (TH), dopamine–ß–hydroxylase (DßH), choline acetyl transferase (ChAT) and vesicular acetylcholine transporter (VAchT). For documentation, light–, fluorescence– and confocal laser scanning microscopy were used. Results: TH–immunoreactive nerve fibres were distinctly surrounding the septum of CRA, but did not form a comprehensive perivascular plexus. These fibres were colocalized with DßH. Further, to a lesser amount, fibres immunoreactive for ChAT and VAchT were present. The vessel wall was lacking fibres immunoreactive for CGRP, SP, and VIP. NADPH–diaphorase reaction showed sparse fibres surrounding CRA. In control experiments, nerve fibres immunoreactive for nNOS were lacking. Conclusions: As demonstrated here, the human CRA shows a distinctive sympathetic and parasympathetic innervation while primary afferent (sensory) innervation was lacking. The absence of VIP and the controversial results concerning nitrergic innervation might be caused due to a downward shift of innervation in the course of the CRA from its origin to the optic nerve head. Further studies have to prove this downward shift and its clinical relevance.
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