scholarly journals Unexpected cone position in 6‐hydroxydopamine‐treated dark‐adapted goldfish retina

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Sophie Thapa ◽  
William Baldridge
Keyword(s):  
6 Hydroxydopamine ◽  
Goldfish Retina

Selective regeneration of photoreceptors in goldfish retina

Development ◽  
1994 ◽  
Vol 120 (9) ◽  
pp. 2409-2419 ◽  
Author(s):  
J.E. Braisted ◽  
T.F. Essman ◽  
P.A. Raymond
Keyword(s):  
Dopaminergic Neurons ◽  
Argon Laser ◽  
Cell Loss ◽  
Specific Class ◽  
Neuronal Progenitors ◽  
Neuroepithelial Cells ◽  
Neuronal Types ◽  
6 Hydroxydopamine ◽  
Goldfish Retina ◽  
Selective Regeneration

Previous work has shown that the neural retina in adult goldfish can regenerate. Following retinal damage elicited by surgical or cytotoxic lesions, missing neurons are replaced by foci of proliferating neuroepithelial cells, which previous studies have suggested are derived from rod precursors. In the intact retina, rod precursors proliferate but produce only new rods. The regenerative responses observed previously have involved replacement of neurons in all retinal layers; selective regeneration of specific neuronal types (except for rod photoreceptors) has not been reported. In the experiments described here, we specifically destroyed either cones alone or cones and rods with an argon laser, and we found that both types of photoreceptors regenerated within a few weeks. The amount of cone regeneration varied in proportion to the degree of rod loss. This is the first demonstration of selective regeneration of a specific class of neuron (i.e., cones) in a region of central nervous tissue where developmental production of that class of neuron has ceased. Selective regeneration may be limited to photoreceptors, however, because when dopaminergic neurons in the inner retina were ablated with intraocular injections of 6-hydroxydopamine, in combination with laser lesions that destroyed photoreceptors, the dopaminergic neurons did not regenerate, but the photoreceptors did. These data support previous studies which showed that substantial cell loss is required to trigger regeneration of inner retinal neurons, including dopaminergic neurons. New observations here bring into question the presumption that rod precursors are the only source of neuronal progenitors during the regenerative response. Finally, a model is presented which suggests a possible mechanism for regulating the phenotypic fate of retinal progenitor cells during retinal regeneration.

Regeneration of dopaminergic neurons in goldfish retina

Development ◽  
1992 ◽  
Vol 114 (4) ◽  
pp. 913-919 ◽  
Author(s):  
J.E. Braisted ◽  
P.A. Raymond
Keyword(s):  
Dopaminergic Neurons ◽  
Developmental Process ◽  
Ganglion Cells ◽  
Outer Nuclear Layer ◽  
Cell Loss ◽  
Cell Types ◽  
High Dose ◽  
Double Labeling ◽  
6 Hydroxydopamine ◽  
Goldfish Retina

The conditions necessary to trigger regeneration of dopaminergic neurons were investigated in the goldfish retina. Intraocular injection of 6-hydroxydopamine (6-OHDA) was used to destroy dopaminergic neurons, and neuronal regeneration was monitored by injections of the thymidine analog bromodeoxyuridine (BUdR). Regenerated dopaminergic neurons, (identified by double-labeling with anti-tyrosine hydroxylase and anti-BUdR antibodies) were found within 3 weeks after 2 injections of 0.6 mg/ml 6-OHDA (estimated intraocular concentration), but not after injection of lower doses. All retinas with regenerated dopaminergic neurons also contained other types of regenerated neurons, including cones and ganglion cells, consistent with nuclear counts which revealed non-selective cell loss (34–36%) in both the outer and inner nuclear layers after exposure to the high dose, but not lower doses of 6-OHDA. Regenerated neurons were produced by clusters of dividing neuroepithelial cells probably derived from rod precursors in the outer nuclear layer. These results demonstrate that dopaminergic neurons will not regenerate after they are selectively ablated but only as part of a developmental process that involves generation of multiple cell types.

Effect of 6-Hydroxydopamine on Neonate Spontaneously Hypertensive and Normotensive Rats

1976 ◽  
Vol 17 (3) ◽  
pp. 419-419 ◽  
Author(s):  
Masayori OZAKI ◽  
Kazunobu SUGAWARA ◽  
Naoko TAKAMI ◽  
Masashi OGAWA ◽  
Masami NIWA
Keyword(s):  
Spontaneously Hypertensive ◽  
6 Hydroxydopamine

Bibliometrics and Visualization of the Mechanisms of Parkinson's Diseases Based on Animal Models

2020 ◽  
Vol 20 (10) ◽  
pp. 1560-1568 ◽  
Author(s):  
Yan-Qiu Wang ◽  
Yi-Bing Chen ◽  
Dong Xu ◽  
Yuan-Lu Cui
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Mitochondrial Protein ◽  
Bibliometric Method ◽  
Metabolism Disorder ◽  
Parkinson’S Diseases ◽  
Model Drug ◽  
6 Hydroxydopamine ◽  
Rats And Mice ◽  
Energy Metabolism Disorder

Objective: Energy metabolism disorder is one of the causes of Parkinson's disease (PD). Rodents, such as rats and mice are often used to establish animal models of PD. This paper used a bibliometric method to analyze the studies of rat and mouse PD models published between 2009 and 2018 in the Web of Science (WOS) database using CiteSpace V software. In addition, we conducted a literature review on the development status and research hotspots in this field in the past ten years. Methods: The related articles on rat and mouse PD models were retrieved from the WOS database, and an analysis of the keywords in these articles was conducted using CiteSpace V. A timeline graph was developed by the software in order to show the focus of researchers in the PD field. Results : A total of 8,636 articles were obtained. Results of the cluster analysis in the PD field such as neuroinflammation, oxidative stress, and autophagy, contributed to the systematic review about the pathogenesis of PD. At the same time, based on the property of the model drug, this review has summarized and compared different administration techniques and mechanisms of 6-hydroxydopamine (6- OHDA), 1-methyl-4-phenyl-1, 2, 4, 5-tetrahydropyridine (MPTP), paraquat and rotenone. Conclusion: According to the bibliometric analysis, studies on PD were focused on the mechanisms of oxidative stress, neuroinflammation, and autophagy. Activated microglia releases inflammatory cytokines; mitochondrial dysfunction is caused by oxidative damage of mitochondrial protein; abnormal autophagy-lysosome pathway can lead to abnormal protein deposition in dopaminergic neurons. In addition, although many animal models of PD have been established, there are some limitations of such models. Therefore, it is necessary to develop models that accurately mimic human PD.

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