Watery and dark axons in Wallerian degeneration of the opossum's optic nerve: different patterns of cytoskeletal breakdown?

Narciso, Marcelo Sampaio; Hokoç, Jan Nora; Martínez, Ana Maria Blanco

doi:10.1590/s0001-37652001000200008

Cited by 30 publications

(38 citation statements)

References 47 publications

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“…Similar to the study using optic nerve crush injury, the current study also identified watery and dark degeneration in the axons [66]. Both patterns were observed at 72 hrs and 7 days of injury.…”

Section: Discussionsupporting

confidence: 85%

Wallerian-like axonal degeneration in the optic nerve after excitotoxic retinal insult: an ultrastructural study

et al. 2010

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BackgroundExcitotoxicity is involved in the pathogenesis of a number neurodegenerative diseases, and axonopathy is an early feature in several of these disorders. In models of excitotoxicity-associated neurological disease, an excitotoxin delivered to the central nervous system (CNS), could trigger neuronal death not only in the somatodendritic region, but also in the axonal region, via oligodendrocyte N-methyl-D-aspartate (NMDA) receptors. The retina and optic nerve, as approachable regions of the brain, provide a unique anatomical substrate to investigate the "downstream" effect of isolated excitotoxic perikaryal injury on central nervous system (CNS) axons, potentially providing information about the pathogenesis of the axonopathy in clinical neurological disorders.Herein, we provide ultrastructural information about the retinal ganglion cell (RGC) somata and their axons, both unmyelinated and myelinated, after NMDA-induced retinal injury. Male Sprague-Dawley rats were killed at 0 h, 24 h, 72 h and 7 days after injecting 20 nM NMDA into the vitreous chamber of the left eye (n = 8 in each group). Saline-injected right eyes served as controls. After perfusion fixation, dissection, resin-embedding and staining, ultrathin sections of eyes and proximal (intraorbital) and distal (intracranial) optic nerve segments were evaluated by transmission electron tomography (TEM).ResultsTEM demonstrated features of necrosis in RGCs: mitochondrial and endoplasmic reticulum swelling, disintegration of polyribosomes, rupture of membranous organelle and formation of myelin bodies. Ultrastructural damage in the optic nerve mimicked the changes of Wallerian degeneration; early nodal/paranodal disturbances were followed by the appearance of three major morphological variants: dark degeneration, watery degeneration and demyelination.ConclusionNMDA-induced excitotoxic retinal injury causes mainly necrotic RGC somal death with Wallerian-like degeneration of the optic nerve. Since axonal degeneration associated with perikaryal excitotoxic injury is an active, regulated process, it may be amenable to therapeutic intervention.

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Section: Discussionsupporting

confidence: 85%

Wallerian-like axonal degeneration in the optic nerve after excitotoxic retinal insult: an ultrastructural study

et al. 2010

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“…The axoplasm degeneration we observed follows the same pattern as that described for vertebrates [Narciso et al, 2001]. It starts by breakdown of microtubules and other axonal organelles.…”

Section: Discussionsupporting

confidence: 82%

“…This indicates an asynchronous pattern of degeneration of nerve fi bers in arthropods, similar to what is observed in vertebrate optic nerve fi bers [Narciso et al, 2001;Marques et al, 2003]. The reason why a certain fi ber starts to degenerate regardless of what is happening to the adjacent similar fi ber is unknown.…”

Section: Discussionsupporting

confidence: 60%

“…The early ultrastructural changes of vertebrate degenerating nerve fi bers after lesion are well known [Martinez, 1999;Narciso et al, 2001] but there are only few reports addressing this subject in arthropods [Blundon et al, 1990;Tanner et al, 1995b]. The most important feature of vertebrate axon degeneration is the early granular disintegration of the axoplasm cytoskeleton due to an increase of intracellular Ca 2+ levels [Martinez and Ribeiro, 1998] and subsequent activation of calcium-dependent prote-ases (calpains).…”

Section: Introductionmentioning

confidence: 99%

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Ultrastructural Study of Normal and Degenerating Nerve Fibers in the Protocerebral Tract of the Crab <i>Ucides cordatus</i>

Corrêa¹,

Allodi²,

Martínez³

2005

Brain Behav Evol

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Wallerian degeneration is a very well described phenomenon in the vertebrate nervous system. In arthropods, and especially in crustaceans, nerve fiber degeneration has not been described extensively. In addition, literature shows that the events do not follow the same patterns as in vertebrates. In this study we report, by qualitative and quantitative ultrastructural analyses, the features and time course of the protocerebral tract degeneration following extirpation of the optic stalk. No remarkable changes were observed seven days after lesion. After 28 days the protocerebral tracts presented apparently preserved small and large diameter axons and some degenerating medium axons, with irregular contours and empty-looking aspect of the axoplasm. Forty days after the ablation of the optic stalks, both small (type I) and medium (type II and III) axons revealed signs of partial or total degeneration, but large nerve fibers (type IV) were still intact. After 45 days, the tract showed signs of advanced stage of degeneration and, apart from large axons, normal-looking fibers were almost absent. At these 3 last time points, degenerating axons displayed different electron densities and aspects, probably correlating to different onset times of the process. In addition, cells with granules in their cytoplasm, possibly hemocytes, were quite distinct, especially at 40 and 45 days after axotomy. These cells might share with glial cells the function of phagocytosis of cellular debris during the protocerebral tract degeneration. Quantitative analysis showed that the number of degenerating fibers increased significantly from 28 to 40 days after lesion, whereas the number of normal fibers decreased accordingly. Measurements of cross-sectional areas of normal and degenerating axons showed that types II and III (medium) start to degenerate before type I (small). Type IV (large) axons do not degenerate, even after 40 days. Therefore, we can conclude that degeneration in these afferent fibers starts late after axotomy, but proceeds at a faster rate afterwards until the complete degeneration of small and medium axons.

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“…This event is called granular disintegration of the axonal cytoskeleton resulting in complete degradation of axonal organelles and proteins and is the main ultra-structural characteristic of axons undergoing WD in the PNS. In central nerve fibers, axon disruption may present in two distinct patterns of axoplasm degeneration, as based on the ultra-structural aspect of the axoplasm (Figure 1) (Narciso et al, 2001). Fig.…”

Section: Overview Of Wallerian Degenerationmentioning

confidence: 99%

Wallerian Degeneration in Injury and Diseases: Concepts and Prevention

Mietto¹,

Costa²,

Lima³

et al. 2011

Advanced Understanding of Neurodegenerative Diseases

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Watery and dark axons in Wallerian degeneration of the opossum's optic nerve: different patterns of cytoskeletal breakdown?

Cited by 30 publications

References 47 publications

Wallerian-like axonal degeneration in the optic nerve after excitotoxic retinal insult: an ultrastructural study

Wallerian-like axonal degeneration in the optic nerve after excitotoxic retinal insult: an ultrastructural study

Ultrastructural Study of Normal and Degenerating Nerve Fibers in the Protocerebral Tract of the Crab <i>Ucides cordatus</i>

Wallerian Degeneration in Injury and Diseases: Concepts and Prevention

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