Axonal Transport Interruption and Anatomy at the Lamina Cribrosa

Radius, Ronald L.; Bade, Bonnie

doi:10.1001/archopht.1982.01030040639017

Cited by 19 publications

(11 citation statements)

References 6 publications

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“…The observation of Minckler et al [6] of organelle accumulation in lamina cribrosa ax ons of the normotensive eye has not been con firmed or denied in subsequent studies, and studies of axoplasmic flow using the move ment of labelled amino acids [7][8][9] did not report blockage in normotensive control eyes. Perhaps for these reasons, the possibility that axoplasmic flow at the optic nerve head is chronically obstructed in the normotensive eye has not been prominent in discussions of the pathogenesis of glaucoma, even in relation to the considerable cohort of glaucoma pa tients in whom IOP is not elevated [3].…”

Section: Introductionmentioning

confidence: 41%

Evidence of Constriction of Optic Nerve Axons at the Lamina cribrosa in the Normotensive Eye in Humans and Other Mammals

et al. 1995

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The ultrastructure of optic nerve axons was examined in several mammals (human, cat, rat, sheep, ox, pig, guinea pig, rabbit). Human material was obtained from normotensive, glaucoma-free eyes and from eyes with a history of glaucoma and raised intra-ocular pressure (IOP). We describe accumulations of organelles (principally mitochondria) in optic nerve axons where they traverse the lamina cribrosa. Accumulations were most prominent in unmyelinated lengths of axons close to lamellae of the lamina cribrosa. Comparable accumulations were not apparent in axons in the retina or optic nerve, suggesting that axoplasmic flow is constricted at the lamina cribrosa. Accumulations were observed both centrally and peripherally to the lamellae, suggesting that flow is constricted in both ortho- and antero-grade directions. Accumulations of organelles were more marked in unmyelinated axons than in adjacent, myelinated axons. In the rabbit, in which most axons are myelinated as they traverse the optic nerve head, organelle accumulations were observed only in a sparse population of unmyelinated axons. In human eyes with a history of raised IOP and glaucoma, the accumulations were abnormally large and frequent and in many axons showed dense-body and fibrillar changes not seen in normotensive eyes. It is suggested that chronic, partial constriction of axoplasmic flow is present at the lamina cribrosa of normotensive eyes in a wide range of mammals, including humans, that the constriction results from the pressure gradient across the lamina cribrosa and that the constriction may be a factor in the many cases of primary glaucoma in which IOP is not raised.

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Section: Introductionmentioning

confidence: 41%

Evidence of Constriction of Optic Nerve Axons at the Lamina cribrosa in the Normotensive Eye in Humans and Other Mammals

et al. 1995

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“…It has been postulated that the structure of the lamina cribrosa may be important in maintaining the integrity of axonal processes (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). For this reason the lamina cribrosa has been implicated as a possible site of damage in glaucoma.…”

Section: Introductionsupporting

confidence: 39%

Quantitative analysis of the lamina cribrosa in vivo using a scanning laser opthalmoscope

Bhandari

Fontana

Fitzke

et al. 1997

Current Eye Research

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“…Pig, cat and dog eyes have a well-developed LC (Coudrillier et al, 2016a; Coudrillier et al, 2016b; Fatehee et al, 2011; Grozdanic et al, 2010; Radius and Bade, 1982a, b), but their ONH vascular anatomy is considerably different to that of the human (De Schaepdrijver et al, 1989; May, 2008). Glaucoma commonly caused by anterior segment dysgenesis and high IOP is a frequent condition seen in cats and dogs (McLellan and Miller, 2011; Pizzirani, 2015).…”

Section: Animal Models Of Glaucomamentioning

confidence: 99%

Biomechanical aspects of axonal damage in glaucoma: A brief review

Tamm

Ethier

Dowling

et al. 2017

Experimental Eye Research

100

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The biomechanical environment within the optic nerve head (ONH) is complex and is likely directly involved in the loss of retinal ganglion cells (RGCs) in glaucoma. Unfortunately, our understanding of this process is poor. Here we describe factors that influence ONH biomechanics, including ONH connective tissue microarchitecture and anatomy; intraocular pressure (IOP); and cerebrospinal fluid pressure (CSFp). We note that connective tissue factors can vary significantly from one individual to the next, as well as regionally within an eye, and that the understanding of ONH biomechanics is hindered by anatomical differences between small-animal models of glaucoma (rats and mice) and humans. Other challenges of using animal models of glaucoma to study the role of biomechanics include the complexity of assessing the degree of glaucomatous progression; and inadequate tools for monitoring and consistently elevating IOP in animal models. We conclude with a consideration of important open research questions/challenges in this area, including: (i) Creating a systems biology description of the ONH; (ii) addressing the role of astrocyte connective tissue remodeling and reactivity in glaucoma; (iii) providing a better characterization of ONH astrocytes and non-astrocytic constituent cells; (iv) better understanding the role of ONH astrocyte phagocytosis, proliferation and death; (v) collecting gene expression and phenotype data on a larger, more coordinated scale; and (vi) developing an implantable IOP sensor.

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Axonal Transport Interruption and Anatomy at the Lamina Cribrosa

Cited by 19 publications

References 6 publications

Evidence of Constriction of Optic Nerve Axons at the Lamina cribrosa in the Normotensive Eye in Humans and Other Mammals

Evidence of Constriction of Optic Nerve Axons at the Lamina cribrosa in the Normotensive Eye in Humans and Other Mammals

Quantitative analysis of the lamina cribrosa in vivo using a scanning laser opthalmoscope

Biomechanical aspects of axonal damage in glaucoma: A brief review

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