The ganglion cell response to optic nerve injury in the cat: differential responses revealed by neurofibrillar staining
The ganglion cell response to optic nerve injury in the cat: differential responses revealed by neurofibrillar staining
The early responses of cat retinal ganglion cells to axotomy have been examined using neurofibrillar and Nissl-stained wholemounts. We were interested to learn whether the enhanced neurofilament expression, seen in a number of neuronal systems, was also present in different neuronal populations of the cat retina and could be used to study the distribution of these cells. We found that beta ganglion cells degenerate very rapidly after axotomy with the nuclei becoming pyknotic within a few days. Few beta cells showed increased neurofibrillar staining of the dendrites. The cell body degenerated prior to any visible degenerative changes in the axon. A proportion of the alpha and gamma ganglion cells degenerated in the first two to three weeks after axotomy. The alpha cells underwent markedly enhanced neurofibrillar staining of their dendrites prior to degeneration. The Nissl material of the cell bodies diminished as the cells degenerated but we have not observed pyknotic nuclei. The dendritic trees of some axotomised gamma cells were also revealed by the neurofibrillar stain three weeks after axotomy. These results show that retinal ganglion cells do not degenerate by a dying back process. We suggest that the rapid degeneration of the beta ganglion cell population comes about by excitotoxic cell death, a consequence of their large glutamatergic input from bipolar cells. The degenerating beta ganglion cells have the morphological appearance of cells undergoing apoptosis.
75-86
Silveira, L.C.L.
c0599953-6274-4a41-8f97-d6b37634581a
Russelakis-Carneiro, M.
51e89362-f101-44e9-b304-4e5ba721ec87
Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4
February 1994
Silveira, L.C.L.
c0599953-6274-4a41-8f97-d6b37634581a
Russelakis-Carneiro, M.
51e89362-f101-44e9-b304-4e5ba721ec87
Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4
Silveira, L.C.L., Russelakis-Carneiro, M. and Perry, V.H.
(1994)
The ganglion cell response to optic nerve injury in the cat: differential responses revealed by neurofibrillar staining.
Journal of Neurocytology, 23 (2), .
(doi:10.1007/BF01183863).
Abstract
The early responses of cat retinal ganglion cells to axotomy have been examined using neurofibrillar and Nissl-stained wholemounts. We were interested to learn whether the enhanced neurofilament expression, seen in a number of neuronal systems, was also present in different neuronal populations of the cat retina and could be used to study the distribution of these cells. We found that beta ganglion cells degenerate very rapidly after axotomy with the nuclei becoming pyknotic within a few days. Few beta cells showed increased neurofibrillar staining of the dendrites. The cell body degenerated prior to any visible degenerative changes in the axon. A proportion of the alpha and gamma ganglion cells degenerated in the first two to three weeks after axotomy. The alpha cells underwent markedly enhanced neurofibrillar staining of their dendrites prior to degeneration. The Nissl material of the cell bodies diminished as the cells degenerated but we have not observed pyknotic nuclei. The dendritic trees of some axotomised gamma cells were also revealed by the neurofibrillar stain three weeks after axotomy. These results show that retinal ganglion cells do not degenerate by a dying back process. We suggest that the rapid degeneration of the beta ganglion cell population comes about by excitotoxic cell death, a consequence of their large glutamatergic input from bipolar cells. The degenerating beta ganglion cells have the morphological appearance of cells undergoing apoptosis.
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Accepted/In Press date: 6 September 1993
Published date: February 1994
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Local EPrints ID: 489598
URI: http://eprints.soton.ac.uk/id/eprint/489598
ISSN: 0300-4864
PURE UUID: aec68cf6-6ce6-4d30-925b-ff89f585d801
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Date deposited: 29 Apr 2024 16:44
Last modified: 05 Jun 2024 17:48
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Author:
L.C.L. Silveira
Author:
M. Russelakis-Carneiro
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