Viability of retinal ganglion cells after optic nerve crush in adult rats

Misantone, Louis J.; Gershenbaum, M.R.; Murray, Marion

doi:10.1007/bf01148334

Cited by 149 publications

(76 citation statements)

References 40 publications

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“…These intraretinal responses are closely associated with the failure of transected mammalian Transection of the optic nerve in adulthood initiates a cascade axons to re-elongate. In contrast to this feature, amphibian and of retrograde neuronal (Ram& y Cajal, 1932;James, 1933; fish optic axons show extensive regrowth and successful reconLiebermann, 197 1; Misantone et al, 1984;Barron et al, 1986) nectivity (for review, see Grafstein, 1986). The sustained in-…”

Section: Discussionmentioning

confidence: 99%

Type-specific stabilization and target-dependent survival of regenerating ganglion cells in the retina of adult rats

Thanos

Mey

1995

J. Neurosci.

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Axotomy-induced degradation of retinal ganglion cells (RGC) can be delayed if the destructive features of activated microglial cells are pharmacologically neutralized, and prevented if the axons are permitted to regrow into transplanted autologous peripheral nerve (PN) pieces. This study was undertaken to classify the regenerating rat RGC and to examine target-dependent effects on survival of subsets of neurons. In analogy to the normal rat retina, we have categorized the retrogradely labeled, regenerating RGC into five classes which are morphologically distinct and reminiscent of normal RGC correlates (types I, II, III, delta-cells, and displaced RGC). Six weeks after transplantation of peripheral nerve to the transected optic nerve, large, type I-like cells (RI) constituted 5.7 +/- 2.0% of the total population. Smaller, round to oval cells of type RII represented the majority of labeled neurons (64.5 +/- 6.1%). Cells of type RIII constituted 4.6 +/- 1.7% of the total population and had very typical, middlesized, polarized perikarya and large dendrites. Less frequent (< 1%) were R-delta and displaced RGC. Transplantation of a PN graft which was not reconnected with a central target (blind-ending group) and monitoring of the extant neurons showed a progressive disappearance of the regenerating RGC, such that 6 months after surgery predominantly few large cells survived. When the retinas were treated with macrophage/microglia- inhibiting factor (MIF), and the regenerating axons were guided into the pretectum, predominantly large RGC of type RI survived. Guidance of the axons into their major natural target, the superior colliculus (SC), resulted in selective survival of many small, RII-like RGC. Calculation of the dendritic coverage factors for the major types of RGC revealed that dendrites of the most abundant small cells of type RII overlapped uniformly and covered the retinal surface completely, whereas cells of types RI and RIII did not suffice for surface coverage. The results suggest that combined suppression of axotomy- induced microglial activation and guidance of regenerating axons with a PN graft into central targets is a suitable technique to produce sufficient numbers of regenerating axons which may retrieve some functional properties. Target-specific neuronal contacts are likely involved in morphological stabilization and better survival of regenerating neurons.

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Section: Discussionmentioning

confidence: 99%

Type-specific stabilization and target-dependent survival of regenerating ganglion cells in the retina of adult rats

Thanos

Mey

1995

J. Neurosci.

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“…Indeed, spontaneous neuronal death has been observed in other B-50/GAP-43-overexpressing transgenic mouse lines (Aigner et al, 1995). In addition, in several neuronal systems injury conditions leading to stronger B-50/ GAP-43 expression and regenerative processes are also associated with a more severe neuronal degeneration (Richardson et al, 1982;Misantone et al, 1984;Villegas-Perez et al, 1988;Bray and Aguayo, 1989;Doster et al, 1991;Tetzlaff et al, 1991Tetzlaff et al, , 1994Herdegen et al, 1997). This suggests that some relationship may link regenerative processes and degenerative phenomena in injured neurons.…”

Section: Transgenic Purkinje Cells Degenerate After Axotomy But Theymentioning

confidence: 98%

Targeted Overexpression of the Neurite Growth-Associated Protein B-50/GAP-43 in Cerebellar Purkinje Cells Induces Sprouting after Axotomy But Not Axon Regeneration into Growth-Permissive Transplants

et al. 1997

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B-50/GAP-43 is a nervous tissue-specific protein, the expression of which is associated with axon growth and regeneration. Its overexpression in transgenic mice produces spontaneous axonal sprouting and enhances induced remodeling in several neuron populations (Aigner et al., 1995;Holtmaat et al., 1995). We examined the capacity of this protein to increase the regenerative potential of injured adult central axons, by inducing targeted B-50/GAP-43 overexpression in Purkinje cells, which normally show poor regenerative capabilities. Thus, transgenic mice were produced in which B-50/GAP-43 overexpression was driven by the Purkinje cell-specific L7 promoter. Uninjured transgenic Purkinje cells displayed normal morphology, indicating that transgene expression does not modify the normal phenotype of these neurons. By contrast, after axotomy numerous transgenic Purkinje cells exhibited profuse sprouting along the axon and at its severed end. Nevertheless, despite these growth phenomena, which never occurred in wild-type mice, the severed transgenic axons were not able to regenerate, either spontaneously or into embryonic neural or Schwann cell grafts placed into the lesion site. Finally, although only a moderate Purkinje cell loss occurred in wild-type cerebella after axotomy, a considerable number of injured transgenic neurons degenerated, but they could be partially rescued by the different transplants placed into the lesion site. Thus, B-50/GAP-43 overexpression substantially modifies Purkinje cell response to axotomy, by inducing growth processes and decreasing their resistance to injury. However, the presence of this protein is not sufficient to enable these neurons to accomplish a full program of axon regeneration.

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“…In these studies, the crush sites at the optic nerve were chosen from 0 to 3 mm behind the globe. [28][29][30][31] Also the device to crush the optic nerve varied between the studies. Buys et al 30 used a Dumont no.…”

Section: Discussionmentioning

confidence: 99%

Dosage dependence of the effect of Ginkgo biloba on the rat retinal ganglion cell survival after optic nerve crush

Zhan

et al. 2008

Eye

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Purpose To investigate the dosage dependence of the Ginkgo biloba effect on retinal ganglion cell survival in the rat optic nerve crush model. Methods The study included 56 SpragueDawley rats, the right optic nerve of which was crushed in a standardized manner. Two hours after the crush and once daily during the follow-up, the animals received intragastral applications of saline (saline group; n ¼ 13), or of a G. biloba extract of 0.25% concentration (n ¼ 14; low-dosage group), 1% concentration (n ¼ 15; medium-dosage group), or 4% concentration (n ¼ 14; high-dosage group). At 23 days after the optic nerve crush, the retinal ganglion cells were retrogradely labelled by injecting 3% fluorogold into the superior colliculi of the brain. At 4 weeks after baseline, the animals were killed. Retinal flat mount photographs were assessed for number and density of the retinal ganglion cells. Results The mean survival rate defined as the ratio of retinal ganglion cell density in the right eye with optic nerve crash divided by the retinal ganglion cell density in left eye without optic nerve intervention increased significantly (Po0.001) from 58.4 ± 9.0% in the saline group to 68.5 ± 5.7% in the low-dosage group, to 73.7 ± 6.4% in the medium-dosage group, and to 74.2 ± 6.8% in the high-dosage group. Conclusions Intragastral applications of a G. biloba extract applied after an experimental and standardized optic nerve crush in rats were associated with a higher survival rate of retinal ganglion cells in a dosage-dependent manner.

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Viability of retinal ganglion cells after optic nerve crush in adult rats

Cited by 149 publications

References 40 publications

Type-specific stabilization and target-dependent survival of regenerating ganglion cells in the retina of adult rats

Type-specific stabilization and target-dependent survival of regenerating ganglion cells in the retina of adult rats

Targeted Overexpression of the Neurite Growth-Associated Protein B-50/GAP-43 in Cerebellar Purkinje Cells Induces Sprouting after Axotomy But Not Axon Regeneration into Growth-Permissive Transplants

Dosage dependence of the effect of Ginkgo biloba on the rat retinal ganglion cell survival after optic nerve crush

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