Ultrastructure of Axonal Reaction in Red Nucleus of CAT

Barron, Kevin D.; Dentinger, Mark P.; Nelson, Louis R.; Mincy, J. Ernest

doi:10.1097/00005072-197505000-00002

Cited by 55 publications

(14 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The numerous vacuoles found by us are possibly cytoplasmic membrane remnants which may be ultimately disposed of by the autophagic activity of lysosomes. Evidence of such autophagy was shown by the presence of undigested material in lysosomes, as noted also by Matthews & Raisman (1972) and Barron et al (1975). (Days 55 to 250) The great majority of remaining neurons in the caudal 200 pm of the red nucleus in the cervical lesion group appeared atrophic from Days 55 to 250.…”

Section: Early Stages (Days 1 To 21)supporting

confidence: 58%

A Light and Electron Microscopic Study of Axon Reaction in the Red Nucleus of the Rat Following Cervical and Thoracic Lesions

Egan

Flumerfelt

Gwyn

1977

Neuropathology Appl Neurobio

View full text Add to dashboard Cite

Egan D.A., Flumerfelt B.A. & Gwyn D.G. (1977) Neuropathology and Applied Neurobiology 3, 423–439 A light and electron microscopic study of axon reaction in the red nucleus of the rat following cervical and thoracic lesions Axon reaction in neurons of the caudal 200 pm of the red nucleus was studied by light and electron microscopy from 1–250 days after axotomy at cervical and at thoracic levels. Following cervical lesions, severe chromatolysis occurred on the third day and by 55 days all of the neurons were atrophic. After thoracic lesions, the reaction was less intense and by 55 days the neurons had returned to normal. The initial morphological changes suggested a regenerative response which was characterized by early dissolution of the ER followed by an increase in its elaboration from the nuclear envelope, and the formation of a nuclear cap. Dilated cisternae of ER were observed in both groups and were seen to contain material similar to that in the ER cisternae generally. Neurofilamentous hyperplasia was most prominent at day 7 in both groups. Neurons of those operated at the cervical level became atrophic at the later stages and signs of autophagy were seen. Evidence of neuronal degeneration, characterized by densely packed whorls, vacuoles and dense bodies, was also seen. The fate of the neuron, i.e. regeneration, atrophy or death, appeared to be determined by the percentage of cytoplasm lost.

show abstract

Section: Early Stages (Days 1 To 21)supporting

confidence: 58%

A Light and Electron Microscopic Study of Axon Reaction in the Red Nucleus of the Rat Following Cervical and Thoracic Lesions

Egan

Flumerfelt

Gwyn

1977

Neuropathology Appl Neurobio

View full text Add to dashboard Cite

show abstract

“…Measurements of YFP + /phospho-c-Jun + neuronal size revealed a reduction in cellular area over time. Further, parallel ultrastructural analyses of axotomized YFP + neurons confirmed that this cell shrinkage was associated with the loss of RER, consistent with ongoing chromatolytic/atrophic alteration (Barron et al, 1975; Barron and Dentinger, 1979; Kreutzberg, 1995). While our previous studies suggested axotomy-mediated atrophic change, their linkage to the actual process of axotomy was indirect (Lifshitz et al, 2007).…”

Section: Discussionmentioning

confidence: 65%

Diffuse Traumatic Axonal Injury in the Mouse Induces Atrophy, c-Jun Activation, and Axonal Outgrowth in the Axotomized Neuronal Population

Greer¹,

McGinn²,

Povlishock³

2011

J. Neurosci.

141

169

View full text Add to dashboard Cite

Traumatic axonal injury (TAI) is a consistent component of traumatic brain injury (TBI), and is associated with much of its morbidity. Little is known regarding the long-term retrograde neuronal consequences of TAI and/or the potential that TAI could lead to anterograde axonal reorganization and repair. To investigate the repertoire of anterograde and retrograde responses triggered by TIA, Thy1-YFP-H mice were subjected to mild central fluid percussion injury and sacrificed at various times between 15 minutes and 28 days post-injury. Based upon confocal assessment of the endogenous neuronal fluorescence, such injury was found to result in diffuse TAI throughout Layer V of the neocortex within YFP+ axons. When these fluorescent approaches were coupled with various quantitative and immunohistochemical approaches we found that this TAI did not result in neuronal death over the 28 day period assessed. Rather, it elicited neuronal atrophy. Within these same axotomized neuronal populations TAI was also found to induce an early and sustained activation of the transcription factors, c-Jun and ATF-3, known regulators of axon regeneration. Parallel ultrastructural studies confirmed these reactive changes consistent with atrophy, in the absence of neuronal death. Concurrent with those events ongoing in the neuronal cell bodies, their downstream axonal segments revealed, as early as 1 day post-injury, morphological changes consistent with reactive sprouting that was accompanied by significant axonal elongation over time. Collectively, these TAI-linked events are consistent with sustained neuronal recovery, an activation of a regenerative genetic program and subsequent axonal reorganization suggestive of some form of regenerative response.

show abstract

“…The recent demonstration of the regenerative capacity of corticospinal fibers of the neonatal hamster after pyramidotomy (46) seems worthy of note in this context. The morphologic expressions of axon reaction in rubral neurons and Betz cells of cat are yery dissimilar (12,13,38), though both are intrinsic nerve cells, subserve a motor function and project to spinal gray through the lateral funiculi. It is likely that such differences in the capacity of two closely related species to regenerate pyramidal fibers are due to divergences in the somal responses of cortical neurons of the two species.…”

Section: Variables Affecting the Axon Reactionmentioning

confidence: 99%

“…3,4)and may persist in apparently recovering cells that exhibit reconstitution of the RER and hypertrophy of the Golgi apparatus some weeks later(13). However, break-up of rosette ribosomes into individual particles and degranulation of cisterns of rough endoplasmic reticulum (RER) are more often encountered in intrinsic neurons (Figs.…”

mentioning

confidence: 99%