Severity of ganglion cell death during early postnatal development is modulated by both neuronal activity and binocular competition

1995 ◽  
Vol 12 (4) ◽  
pp. 605-610 ◽  
Author(s):  
A.J. Scheetz ◽  
Robert W. Williams ◽  
Mark W. Dubin
Keyword(s):  
Cell Death ◽  
Ganglion Cell ◽  
Neuronal Activity ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Population Declines ◽  
Neuron Death ◽  
Early Postnatal Development ◽  
Naturally Occurring ◽  
Ganglion Cell Death

AbstractThe influence of postnatal neuronal activity on the magnitude of retinal ganglion cell death has been studied in cats. A constant blockade of activity in one eye starting just after birth does not change the severity of naturally occurring ganglion cell death, and as in normal animals, the ganglion cell population declines from 250,000 to 160,000 over a 4- to 6-week period. However, the population of retinal ganglion cells in the active untreated eye of monocularly deprived cats is increased 12% above normal (180,000 vs. 160,000 in each of four cases). This increase of 20,000 cells is permanent, and presumably reflects the competitive advantage in their target nuclei that the still active axons have over their silenced companions from the treated eye. Surprisingly, in one animal treated successfully for long duration with TTX in both eyes, the population of ganglion cells was elevated in both eyes (200,000 and 208,000 ganglion cells). This increase matches that achieved by early unilateral enucleation (Williams et al., 1983). Our results demonstrate that the complete blockade of activity reduces the severity of naturally occurring cell death in a population of CNS sensory neurons. The effects of unilateral blockade emphasize that the activity-dependent modulation of neuron death only occurs under conditions that do not place the inactive population of neurons at a competitive disadvantage.

scholarly journals Neuroprotective and Anti-Inflammatory Effects of a Hydrophilic Saffron Extract in a Model of Glaucoma

2019 ◽  
Vol 20 (17) ◽  
pp. 4110 ◽  
Author(s):  
Jose A. Fernández-Albarral ◽  
Ana I. Ramírez ◽  
Rosa de Hoz ◽  
Nerea López-Villarín ◽  
Elena Salobrar-García ◽  
...  
Keyword(s):  
Cell Death ◽  
Intraocular Pressure ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Retinal Ganglion Cell Death ◽  
Saffron Extract ◽  
Anti Inflammatory ◽  
Ganglion Cell Death

Glaucoma is a neurodegenerative disease characterized by the loss of retinal ganglion cells (RGCs). An increase in the intraocular pressure is the principal risk factor for such loss, but controlling this pressure does not always prevent glaucomatous damage. Activation of immune cells resident in the retina (microglia) may contribute to RGC death. Thus, a substance with anti-inflammatory activity may protect against RGC degeneration. This study investigated the neuroprotective and anti-inflammatory effects of a hydrophilic saffron extract standardized to 3% crocin content in a mouse model of unilateral, laser-induced ocular hypertension (OHT). Treatment with saffron extract decreased microglion numbers and morphological signs of their activation, including soma size and process retraction, both in OHT and in contralateral eyes. Saffron extract treatment also partially reversed OHT-induced down-regulation of P2RY12. In addition, the extract prevented retinal ganglion cell death in OHT eyes. Oral administration of saffron extract was able to decrease the neuroinflammation associated with increased intraocular pressure, preventing retinal ganglion cell death. Our findings indicate that saffron extract may exert a protective effect in glaucomatous pathology.

A second episode of ganglion cell death takes place when an optic nerve regenerates for a second time in the frog

1993 ◽  
Vol 10 (2) ◽  
pp. 297-301 ◽  
Author(s):  
L. D. Beazley ◽  
J.E. Darby
Keyword(s):  
Cell Death ◽  
Optic Nerve ◽  
Ganglion Cell ◽  
Ganglion Cells ◽  
Cresyl Violet ◽  
Retinal Ganglion ◽  
Nerve Crush ◽  
Optic Nerve Regeneration ◽  
Ability To Regenerate ◽  
Ganglion Cell Death

AbstractWe have previously reported that during optic nerve regeneration in the frog, 30–40% of retinal ganglion cells die, the loss being complete within 10 weeks. In the present study, we crushed the optic nerve, waited 10 weeks, and then recrushed the nerve at the same site. Retinae were examined 10 weeks later. We estimated ganglion cell numbers from cresyl-violet-stained wholemounts and found a fall of 53% compared to normals. The loss was significantly greater than the losses of 36% and 35%, respectively, in frogs which received a single optic nerve crush and were examined 10 or 20–24 weeks later. The results indicate that a second episode of ganglion cell death took place when the optic nerve regenerated a second time. We conclude that ganglion cells in the frog are not comprised of two subpopulations, only one of which intrinsically possesses the ability to regenerate.

The autoregulation of retinal ganglion cell number

Development ◽  
2001 ◽  
Vol 128 (1) ◽  
pp. 117-124 ◽  
Author(s):  
M. Gonzalez-Hoyuela ◽  
J.A. Barbas ◽  
A. Rodriguez-Tebar
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Ganglion Cell ◽  
Ganglion Cell Layer ◽  
Ganglion Cells ◽  
Cell Layer ◽  
Cell Number ◽  
Retinal Ganglion ◽  
Cell Ablation ◽  
Ganglion Cell Death

The development of the nervous system is dependent on a complex set of signals whose precise co-ordination ensures that the correct number of neurones are generated. This regulation is achieved through a variety of cues that influence both the generation and the maintenance of neurones during development. We show that in the chick embryo, stratified retinal ganglion cells (RGCs) are themselves responsible for providing the signals that control the number of RGCs that are generated, both by inhibiting the generation of new ganglion cells and by killing incoming migratory ganglion cells. Selective toxicological ablation of RGCs in the chick embryo resulted in the achronic generation of ganglion cells, which eventually led to the repopulation of the ganglion cell layer and a large decrease in the physiological cell death affecting postmitotic migratory neurones. Interestingly, the application of exogenous NGF reversed the effects of ganglion cell ablation on ganglion cell death. Because the only source of NGF in the retina is that produced by the stratified ganglion cells, we infer that these differentiated neurones regulate their own cell number by secreting NGF, a neurotrophin that has previously been shown to be responsible for the death of migrating ganglion cells.

Naturally occurring and induced ganglion cell death

1986 ◽  
Vol 174 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Sandra Jenkins ◽  
Charles Straznicky
Keyword(s):  
Cell Death ◽  
Ganglion Cell ◽  
Naturally Occurring ◽  
Ganglion Cell Death
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