Origin of myelinated nerves in the rat iris

Huhtala, Antero

doi:10.1016/0014-4835(76)90053-1

Cited by 47 publications

(10 citation statements)

References 14 publications

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“…Thus, removal of the main ciliary ganglion, together with ocular sensory and sympathetic denervation does not completely eliminate corneal (present study, Fig. 7) and iridial (Huhtala, 1976 ;Bjo$ rklund et al, 1985) nerve fibers.…”

Section: Retrograde Tracing Studies : Origins Of Corneal Parasympathementioning

confidence: 71%

Parasympathetic Innervation of the Rat Cornea

Marfurt

Jones

Thrasher

1998

Experimental Eye Research

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Section: Retrograde Tracing Studies : Origins Of Corneal Parasympathementioning

confidence: 71%

Parasympathetic Innervation of the Rat Cornea

Marfurt

Jones

Thrasher

1998

Experimental Eye Research

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“…This recovery period is based on prior studies in rats in which sympathetic terminals underwent complete structural degeneration 7 days after SCGX. 24 However, successful SCGX surgery was easily confirmed on clinical examination just a few hours after the surgery, as the sympathectomized side developed ptosis and its pupil lost the ability to dilate in the dark.…”

Section: Surgical Removal Of the Superior Cervical Ganglionmentioning

confidence: 99%

Surgical Denervation of Ocular Sympathetic Afferents Decreases Local Transforming Growth Factor-β and Abolishes Immune Privilege

Vega

Keino

Masli

2009

The American Journal of Pathology

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Mounting evidence points to a role for the sympathetic nervous system in suppressing inflammation. This role might be of specific relevance for immune privilege in the eye, where, sporadically, patients with denervated sympathetic fibers develop chronic inflammation. The present study used mice to investigate whether the robust innervation of intraocular structures by the sympathetic system plays a role in maintaining ocular immune privilege. We first performed surgical removal of the superior cervical ganglion, which supplies sympathetic fibers to the eye, and studied the immune response generated against soluble antigens or allogeneic tumor cells injected into the ocular anterior chamber under these conditions. Our results show that in the absence of functional sympathetic fibers, the eye loses its ability to prevent either the immune rejection of intraocular allogeneic tumor cells or the suppression of delayed type hypersensitivity responses against soluble antigens injected in the anterior chamber. This loss of immune privilege is accompanied by a decrease in the concentration of transforming growth factor-␤ in the aqueous humor. These results suggest that immune privilege is lost in the absence of a functional sympathetic innervation of the eye, allowing intraocular immune responses to become exaggerated. We conclude that ocular sympathetic nerves are critical for the generation and maintenance of immune privilege in the eye through the facilitation of local transforming growth factor

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“…A unique feature of this model is that two distant tissues are attacked at the same time. Both tissues, the spinal cord and the iris, contain MBP that may be targeted by encephalitogenic T cells (Huhtala, 1976;Steinman, 1996). Thus, cells of similar phenotype (V␤8.2 ϩ and OX40 ϩ CD4 ϩ T cells) and antigen specificity to MBP pathogenic epitopes may be regulated by a similar regulatory mechanism to let them enter the spinal cord and the eye.…”

Section: Discussionmentioning

confidence: 97%

“…Possible target antigens are myelinated neurons in CNS and iris. Uveitis possibly results from the primary reaction to myelinated nerves in the iris, which exist there in quite abundant quantity (Huhtala, 1976).…”

Section: Introductionmentioning

confidence: 99%

Similar pattern of MCP-1 expression in spinal cords and eyes of Lewis rats with experimental autoimmune encephalomyelitis associated anterior uveitis

et al. 1997

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Monocyte chemoattractant protein-1 (MCP-1) is a member of the CC chemokine family responsible for the recruitment of T cells that have been found during inflammation of the spinal cord in experimental autoimmune encephalomyelitis (EAE) in Lewis rats immunized with myelin basic protein (MBP). Lewis rats injected with MBP also developed anterior uveitis (AU), which coincided with the onset of EAE. In the present studies, we examined the expression and distribution of MCP-1 in the eye and spinal cord during disease and compared it to the expression of Th1 cell type cytokines. Initially, MCP-1 expression was detected at the preclinical phase in the iris/ciliary body and lumbar spinal cord and increased during the course of EAE/AU. Mononuclear infiltrating cells and endothelial cells and astrocytes of the CNS could be identified as a source of MCP-1 by in situ hybridization. Kinetics of expression of Th1 characteristic cytokines such as IL-2 and IFNgamma was in agreement with the expression of MCP-1 chemokine. Moreover, induction of the gene expression of MCP-1 seemed to occur earlier than that of MIP-2, and it correlated with increasing disease severity. MCP-1 seems to contribute to the initial recruitment of inflammatory cells into both the tissues of the eye and CNS over the course of disease.

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Origin of myelinated nerves in the rat iris

Cited by 47 publications

References 14 publications

Parasympathetic Innervation of the Rat Cornea

Parasympathetic Innervation of the Rat Cornea

Surgical Denervation of Ocular Sympathetic Afferents Decreases Local Transforming Growth Factor-β and Abolishes Immune Privilege

Similar pattern of MCP-1 expression in spinal cords and eyes of Lewis rats with experimental autoimmune encephalomyelitis associated anterior uveitis

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