Electron Microscopy of the Mouse Optic Nerve: A Quantitative Study of the Total Optic Nerve Fibers

Honjin, Ryohei; Sakato, S; Yamashita, Toshio

doi:10.1679/aohc1950.40.321

Cited by 39 publications

(29 citation statements)

References 15 publications

(10 reference statements)

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“…The diameter range in Tupaia is close to that reported for other mammals of similar size (Honjin et al, 1977;Hughes, 1977;Freeman and Watson, 1978;Rhoades et al, 1979;Guy et al, 1989). With respect to the mode and the average, however, similar values are found only in the chipmunk, the mouse, and rat (Honjin et al 1977;Hughes, 1977;Wakakuwa et al, 1987).…”

Section: Fiber and Axon Diameterssupporting

confidence: 88%

Classes of axons and their distribution in the optic nerve of the tree shrew (Tupaia belangeri)

Drenhaus¹,

Gunten²,

Rager³

1997

Anat. Rec.

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Section: Fiber and Axon Diameterssupporting

confidence: 88%

Classes of axons and their distribution in the optic nerve of the tree shrew (Tupaia belangeri)

Drenhaus¹,

Gunten²,

Rager³

1997

Anat. Rec.

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“…Even within these ranges, a significant portion of the axons in the human optic nerve are likely to experience ATP shortfall if the model accurately predicts energy availability. The same is true for mouse, with a frequency distribution of optic nerve fiber diameter that peaks at 0.7–0.9 μm; 50.4% of axons are 0.9 um in diameter or less (Honjin et al, 1977), suggesting that there could also be a mitochondrial-derived ATP shortfall in a large subset of axons. The energy sufficiency calculations also depend upon the axon having enough access to glucose.…”

Section: Energy In Axonsmentioning

confidence: 86%

Metabolic Vulnerability in the Neurodegenerative Disease Glaucoma

Inman

Harun‐Or‐Rashid

2017

Front. Neurosci.

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Axons can be several orders of magnitude longer than neural somas, presenting logistical difficulties in cargo trafficking and structural maintenance. Keeping the axon compartment well supplied with energy also presents a considerable challenge; even seemingly subtle modifications of metabolism can result in functional deficits and degeneration. Axons require a great deal of energy, up to 70% of all energy used by a neuron, just to maintain the resting membrane potential. Axonal energy, in the form of ATP, is generated primarily through oxidative phosphorylation in the mitochondria. In addition, glial cells contribute metabolic intermediates to axons at moments of high activity or according to need. Recent evidence suggests energy disruption is an early contributor to pathology in a wide variety of neurodegenerative disorders characterized by axonopathy. However, the degree to which the energy disruption is intrinsic to the axon vs. associated glia is not clear. This paper will review the role of energy availability and utilization in axon degeneration in glaucoma, a chronic axonopathy of the retinal projection.

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“…In short, several decades of theoretical and experimental data suggest that, from the perspective of conduction velocity alone, an ‘optimum profile’ of myelin throughout the nervous system exists, a process that was thought to be achieved during development. In some regions of the nervous system such as the optic nerve, the parameters of myelin microstructure do approach these ideal proportions (Honjin et al, 1977). In other regions, however, such as the cortex and subcortical projections, myelin profiles are sub-“ideal” (Peters and Sethares, 1996; Tomassy et al, 2014), a state that may render these regions more amenable to plastic, experience-dependent changes.…”

mentioning

confidence: 99%