scholarly journals Independent modes of ganglion cell translocation ensure correct lamination of the zebrafish retina

2016 ◽  
Author(s):  
Jaroslav Icha ◽  
Christiane Grunert ◽  
Mauricio Rocha-Martins ◽  
Caren Norden
Keyword(s):  
Nervous System ◽  
Optic Nerve ◽  
Ganglion Cell ◽  
Light Sheet ◽  
Retinal Layer ◽  
Layer Formation ◽  
Neuronal Connectivity ◽  
Basal Process ◽  
Light Sheet Microscopy ◽  
And Function

AbstractThe arrangement of neurons into distinct layers is critical for neuronal connectivity and function of the nervous system. During development, most neurons move from their birthplace to the appropriate layer, where they polarize. However, kinetics and modes of many neuronal translocation events still await exploration. Here, we investigate ganglion cell (RGC) translocation across the embryonic zebrafish retina. After completing their translocation, RGCs establish the most basal retinal layer where they form the optic nerve. Using in toto light sheet microscopy, we show that somal translocation of RGCs is a fast and directed event. It depends on basal process attachment and stabilized microtubules. Interestingly, interference with somal translocation induces a switch to multipolar migration. This multipolar mode is less efficient but still leads to successful RGC layer formation. When both modes are inhibited, RGCs that fail to translocate induce lamination defects, indicating that correct RGC translocation is crucial for subsequent retinal lamination.

scholarly journals Independent modes of ganglion cell translocation ensure correct lamination of the zebrafish retina

2016 ◽  
Vol 215 (2) ◽  
pp. 259-275 ◽  
Author(s):  
Jaroslav Icha ◽  
Christiane Kunath ◽  
Mauricio Rocha-Martins ◽  
Caren Norden
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Light Sheet ◽  
Retinal Layer ◽  
Retinal Ganglion ◽  
Layer Formation ◽  
Neuronal Connectivity ◽  
Light Sheet Microscopy ◽  
And Function

The arrangement of neurons into distinct layers is critical for neuronal connectivity and function. During development, most neurons move from their birthplace to the appropriate layer, where they polarize. However, kinetics and modes of many neuronal translocation events still await exploration. In this study, we investigate retinal ganglion cell (RGC) translocation across the embryonic zebrafish retina. After completing their translocation, RGCs establish the most basal retinal layer where they form the optic nerve. Using in toto light sheet microscopy, we show that somal translocation of RGCs is a fast and directed event. It depends on basal process attachment and stabilized microtubules. Interestingly, interference with somal translocation induces a switch to multipolar migration. This multipolar mode is less efficient but still leads to successful RGC layer formation. When both modes are inhibited though, RGCs fail to translocate and induce lamination defects. This indicates that correct RGC translocation is crucial for subsequent retinal lamination.

scholarly journals ADVANCED OPTICAL TECHNIQUES TO EXPLORE BRAIN STRUCTURE AND FUNCTION

2013 ◽  
Vol 06 (01) ◽  
pp. 1230002 ◽  
Author(s):  
L. SILVESTRI ◽  
A. L. ALLEGRA MASCARO ◽  
J. LOTTI ◽  
L. SACCONI ◽  
F. S. PAVONE
Keyword(s):  
Brain Structure ◽  
Light Sheet ◽  
Structure And Function ◽  
Optical Methods ◽  
Optical Techniques ◽  
Time Dynamics ◽  
Light Sheet Microscopy ◽  
Brain Structure And Function ◽  
Complex Relationships ◽  
And Function

Understanding brain structure and function, and the complex relationships between them, is one of the grand challenges of contemporary sciences. Thanks to their flexibility, optical techniques could be the key to explore this complex network. In this manuscript, we briefly review recent advancements in optical methods applied to three main issues: anatomy, plasticity and functionality. We describe novel implementations of light-sheet microscopy to resolve neuronal anatomy in whole fixed brains with cellular resolution. Moving to living samples, we show how real-time dynamics of brain rewiring can be visualized through two-photon microscopy with the spatial resolution of single synaptic contacts. The plasticity of the injured brain can also be dissected through cutting-edge optical methods that specifically ablate single neuronal processes. Finally, we report how nonlinear microscopy in combination with novel voltage sensitive dyes allow optical registrations of action potential across a population of neurons opening promising prospective in understanding brain functionality. The knowledge acquired from these complementary optical methods may provide a deeper comprehension of the brain and of its unique features.

scholarly journals SPED Light Sheet Microscopy: Fast Mapping of Biological System Structure and Function

Cell ◽  
2015 ◽  
Vol 163 (7) ◽  
pp. 1796-1806 ◽  
Author(s):  
Raju Tomer ◽  
Matthew Lovett-Barron ◽  
Isaac Kauvar ◽  
Aaron Andalman ◽  
Vanessa M. Burns ◽  
...  
Keyword(s):  
Biological System ◽  
Light Sheet ◽  
Structure And Function ◽  
System Structure ◽  
Fast Mapping ◽  
Light Sheet Microscopy ◽  
And Function

scholarly journals Retinal ganglion cell loss in an ex vivo mouse model of optic nerve cut is prevented by curcumin treatment

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Lucia Buccarello ◽  
Jessica Dragotto ◽  
Kambiz Hassanzadeh ◽  
Rita Maccarone ◽  
Massimo Corbo ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Degeneration ◽  
Retinal Ganglion Cell ◽  
Time Window ◽  
Ex Vivo ◽  
Nerve Degeneration ◽  
Retinal Cell ◽  
Retinal Layer ◽  
Retinal Ganglion

AbstractRetinal ganglion cell (RGC) loss is a pathologic feature common to several retinopathies associated to optic nerve damage, leading to visual loss and blindness. Although several scientific efforts have been spent to understand the molecular and cellular changes occurring in retinal degeneration, an effective therapy to counteract the retinal damage is still not available. Here we show that eyeballs, enucleated with the concomitant optic nerve cut (ONC), when kept in PBS for 24 h showed retinal and optic nerve degeneration. Examining retinas and optic nerves at different time points in a temporal window of 24 h, we found a thinning of some retinal layers especially RGC’s layer, observing a powerful RGC loss after 24 h correlated with an apoptotic, MAPKs and degradative pathways dysfunctions. Specifically, we detected a time-dependent increase of Caspase-3, -9 and pro-apoptotic marker levels, associated with a strong reduction of BRN3A and NeuN levels. Importantly, a powerful activation of JNK, c-Jun, and ERK signaling (MAPKs) were observed, correlated with a significant augmented SUMO-1 and UBC9 protein levels. The degradation signaling pathways was also altered, causing a significant decrease of ubiquitination level and an increased LC3B activation. Notably, it was also detected an augmented Tau protein level. Curcumin, a powerful antioxidant natural compound, prevented the alterations of apoptotic cascade, MAPKs, and SUMO-1 pathways and the degradation system, preserving the RGC survival and the retinal layer thickness. This ex vivo retinal degeneration model could be a useful method to study, in a short time window, the effect of neuroprotective tools like curcumin that could represent a potential treatment to contrast retinal cell death.

scholarly journals Heterozygous mutation of Vegfr3 decreases renal lymphatics but is dispensable for renal function

2021 ◽  
Author(s):  
Hao Liu ◽  
Chitkale Hiremath ◽  
Quinten Patterson ◽  
Saumya Vora ◽  
Zhiguo Shang ◽  
...  
Keyword(s):  
Renal Function ◽  
Kidney Disease ◽  
Lymphatic Vessels ◽  
Light Sheet ◽  
Structure And Function ◽  
Heterozygous Mutation ◽  
Light Sheet Microscopy ◽  
Perivascular Inflammation ◽  
Lymphatic Density ◽  
And Function

ABSTRACTBackgroundLymphatic abnormalities are observed in several types of kidney disease, but the relationship between the renal lymphatic system and renal function is unclear. The discovery of lymphatic-specific proteins, advances in microscopy, and available genetic mouse models provide the tools to help elucidate the role of renal lymphatics in physiology and disease.MethodsWe utilized a mouse model containing a missense mutation in Vegfr3 (dubbed Chy) that abrogates its kinase ability. Vegfr3Chy/+ mice were examined for developmental abnormalities and kidney-specific outcomes. Control and Vegfr3Chy/+ mice were subjected to cisplatin-mediated injury. We characterized renal lymphatics using a combination of tissue clearing, light-sheet microscopy and computational analyses.ResultsIn the kidney, we found Vegfr3 is expressed not only in lymphatic vessels, but also various blood vessels. Vegfr3Chy/+ mice had severely reduced renal lymphatics with 100% penetrance, but we found no abnormalities in blood pressure, renal function and histology. Similarly, there was no difference in the degree of renal injury after cisplatin, although Vegfr3Chy/+ mice developed more perivascular inflammation by histology. Control mice treated with cisplatin had a measurable increase in cortical lymphatic density despite no change in cortical lymphatic volume and length.ConclusionsWe demonstrate that Vegfr3 is required for development of renal lymphatics, but a reduction in lymphatic density does not alter renal function and induces only modest histological changes after injury. Our data suggests that an increase in lymphatic density after cisplatin injury may reflect the loss of cortical volume associated with chronic kidney disease rather than growth of lymphatic vessels.SIGNIFICANCE STATEMENTDefects in renal lymphatics occur in various kidney diseases, but their role in maintaining kidney structure and function is unknown. We combine tissue clearing, light-sheet microscopy and computational analysis to characterize lymphatics and find that mice with a heterozygous mutation in Vegfr3 (Vegfr3Chy/+) have severely reduced renal lymphatics. Strikingly, these mice have indistinguishable renal function and histology compared with controls. Even after cisplatin injury, there are no differences in renal function, although Vegfr3Chy/+ mice developed more perivascular inflammation. Our data present a novel method of lymphatic quantification and suggest that a normal complement of renal lymphatics is dispensable for renal structure and function.

Carvedilol Promotes Retinal Ganglion Cell Survival Following Optic Nerve Injury via ASK1-p38 MAPK Pathway

2020 ◽  
Vol 18 (9) ◽  
pp. 695-704 ◽  
Author(s):  
Bei Liu ◽  
Yu-Jia Liu
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Nerve Injury ◽  
Retinal Ganglion Cell ◽  
Mapk Pathway ◽  
Mitogen Activated Protein Kinase ◽  
Ganglion Cell Complex ◽  
Retinal Layer ◽  
Retinal Ganglion ◽  
Optic Nerve Injury

Background: Carvedilol, which is considered as a nonselective β-adrenoreceptor blocker, has many pleiotropic activities. It also causes great impact on neuroprotection because of its antioxidant ability, which suggested that carvedilol may be effective in protecting RGCs from increased oxidative stress. Objective: To examine the effects of carvedilol on preventing Retinal Ganglion Cell (RGC) death in a mouse model of Optic Nerve Injury (ONI). Methods: C57BL/6J mice were subjected to Optic Nerve Injury (ONI) model and treated with carvedilol or placebo. Histological and morphometric studies were performed; the RGC number, the amount of neurons in the ganglion cell layer and the thickness of the Inner Retinal Layer (IRL) was quantified. The average thickness of Ganglion Cell Complex (GCC) was determined by the Spectral- Domain OCT (SD-OCT) assay. Immunohistochemistry, western blot and quantitative real-time PCR analysis were also applied. Results: Daily treatment of carvedilol reduced RGC death following ONI, and in vivo retinal imaging revealed that carvedilol can effectively prevent retinal degeneration. The expression of chemokines important for micorglia recruitment was deceased with carvedilol ingestion and the accumulation of retinal microglia is reduced consequently. In addition, the ONI-induced expression of inducible nitric oxide synthase in the retina was inhibited with carvedilol treatment in the retina. We also discovered that carvedilol suppressed ONI-induced activation of Apoptosis Signal-regulating Kinase-1 (ASK1) and p38 Mitogen-Activated Protein Kinase (MAPK) pathway. Conclusion: The results of this study indicate that carvedilol can stimulate neuroprotection and neuroregeneration, and may be useful for treatment of various neurodegenerative diseases.

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