Programmed Cell Death in Zebrafish Rohon Beard Neurons Is Influenced by TrkC1/NT-3 Signaling

Williams, Jennifer A. E.; Barrios, Arantza; Gatchalian, Christine L.; Rubin, Lee L.; Wilson, Stephen W.; Holder, Nigel

doi:10.1006/dbio.2000.9860

Cited by 95 publications

(110 citation statements)

References 36 publications

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“…Previous studies provided evidence that zebrafish RBs undergo programmed cell death and are essentially gone by the end of 3d (Williams et al, 2000;Svoboda et al, 2001;Cole and Ross, 2001). Thus, we were surprised that our labeled cells remained for as long as 7d.…”

Section: Rbs Fragment Their Dna Before Overt Cellular Degenerationmentioning

confidence: 99%

“…In zebrafish, some RBs fragment their DNA before DRG axogenesis, thus Williams et al (2000) suggested it was unlikely that early RB death is due to direct interactions with DRG neurons. However, the possibility remains that some interaction with DRG neurons triggers later-occurring RB death.…”

Section: Rb Cell Death Is Independent Of Drg Formationmentioning

confidence: 99%

“…Zebrafish RBs share the same attributes as amphibian RBs: large cell bodies with huge nuclei and granular cytoplasm (Metcalfe et al, 1990). As in amphibians, zebrafish RBs die over a protracted period of time (Williams et al, 2000;Cole and Ross, 2001). Thus, several different factors may contribute to the demise of these cells.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, several different factors may contribute to the demise of these cells. It has been shown recently that zebrafish RB death is correlated with reduced expression of trkC1, suggesting that RB survival involves the neurotrophin NT-3 (Williams et al, 2000). RB death also appears delayed by inhibiting caspase activity, suggesting that RB death is caspase-dependent (Williams et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Slow degeneration of zebrafish Rohon‐Beard neurons during programmed cell death

Reyes

Haendel

Grant

et al. 2003

Developmental Dynamics

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Rohon-Beard cells are large, mechanosensory neurons located in the dorsal spinal cord of anamniote vertebrates. In most species studied to date, these cells die during development. We followed labeled Rohon-Beard cells in living zebrafish embryos and found that they degenerate slowly, over many days. During degeneration, the soma shrinks and finally disappears, and the processes become beady in appearance and finally break apart, but they do not retract. Zebrafish Rohon-Beard cells apparently fragment their DNA, as revealed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) labeling, before undergoing degenerative morphologic changes. We also followed the development of labeled dorsal root ganglion neurons, as they are developing at the same stages that Rohon-Beard cells are degenerating. We found that, although axons of both cell types extend into similar regions, Rohon-Beard cells degenerate normally in mutants lacking dorsal root ganglia, providing evidence that interactions between the two cell types are not responsible for Rohon-Beard cell degeneration. Developmental Dynamics 229:30 -41, 2004.

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Section: Rbs Fragment Their Dna Before Overt Cellular Degenerationmentioning

confidence: 99%

Section: Rb Cell Death Is Independent Of Drg Formationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Slow degeneration of zebrafish Rohon‐Beard neurons during programmed cell death

Reyes

Haendel

Grant

et al. 2003

Developmental Dynamics

View full text Add to dashboard Cite

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“…Zebrafish RB neurons are the equivalent of the amphibian RB neurons, having large cell bodies with huge nuclei and granular cytoplasm (Metcalfe et al, 1990). Although zebrafish RB neurons begin showing signs of programmed cell death, such as DNA fragmentation, as early as the first day of development, the cells remain present for considerably longer and degenerate over a protracted period of time and unlike in amphibians, independent of any developmental link to DRG neurons (Williams et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Cuevas

Trickler

Guo

et al. 2013

Neurotoxicology and Teratology

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Ketamine, a non-competitive antagonist of N-methyl-D-aspartate (NMDA) type glutamate receptors is commonly used as a pediatric anesthetic. Multiple studies have shown ketamine to be neurotoxic, particularly when administered during the brain growth spurt. Previously, we have shown that ketamine is detrimental to motor neuron development in the zebrafish embryos. Here, using both wild type (WT) and transgenic (hb9:GFP) zebrafish embryos, we demonstrate that ketamine is neurotoxic to both motor and sensory neurons. Drug absorption studies showed that in the WT embryos, ketamine accumulation was approximately 0.4% of the original dose added to the exposure medium. The transgenic embryos express green fluorescent protein (GFP) localized in the motor neurons making them ideal for evaluating motor neuron development and toxicities in vivo. The hb9:GFP zebrafish embryos (28 h post fertilization) treated with 2 mM ketamine for 20 h demonstrated significant reductions in spinal motor neuron numbers, while co-treatment with acetyl L-carnitine proved to be neuroprotective. In whole mount immunohistochemical studies using WT embryos, a similar effect was observed for the primary sensory neurons. In the ketamine-treated WT embryos, the number of primary sensory Rohon-Beard (RB) neurons was significantly reduced compared to that in controls. However, acetyl L-carnitine co-treatment prevented ketamine-induced adverse effects on the RB neurons. These results suggest that acetyl L-carnitine protects both motor and sensory neurons from ketamine-induced neurotoxicity.

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Degeneration and regeneration of ultraviolet cone photoreceptors during development in rainbow trout

Allison

Dann

Veldhoen

et al. 2006

J of Comparative Neurology

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Ultraviolet-sensitive (UVS) cones disappear from the retina of salmonid fishes during a metamorphosis that prepares them for deeper/marine waters. UVS cones subsequently reappear in the retina near sexual maturation and the return migration to natal streams. Cellular mechanisms of this UVS cone ontogeny were investigated using electroretinograms, in situ hybridization, and immunohistochemistry against opsins during and after thyroid hormone (TH) treatments of rainbow trout (Oncorhynchus mykiss). Increasing TH levels led to UVS cone degeneration. Labeling demonstrated that UVS cone degeneration occurs via programmed cell death and caspase inhibitors can inhibit this death. After the cessation of TH treatment, UVS cones regenerated in the retina. Bromodeoxyuridine (BrdU) was applied after the termination of TH treatment and was detected in the nuclei of cells expressing UVS opsin. BrdU was found in UVS cones but not other cone types. The most parsimonious explanation for the data is that UVS cones degenerated and UVS cones were regenerated from intrinsic retinal progenitor cells. Regenerating UVS cones were functionally integrated such that they were able to elicit electrical responses from second-order neurons. This is the first report of cones regenerating during natural development. Both the death and regeneration of cones in retinae represent novel mechanisms for tuning visual systems to new visual tasks or environments.

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Programmed Cell Death in Zebrafish Rohon Beard Neurons Is Influenced by TrkC1/NT-3 Signaling

Cited by 95 publications

References 36 publications

Slow degeneration of zebrafish Rohon‐Beard neurons during programmed cell death

Slow degeneration of zebrafish Rohon‐Beard neurons during programmed cell death

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Degeneration and regeneration of ultraviolet cone photoreceptors during development in rainbow trout

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