Embryonic Hyperglycemia Delays the Development of Retinal Synapses in a Zebrafish Model
Abhishek P Shrestha1, Ambalavanan Saravanakumar1,2, Bridget Konadu3
1Department of Pharmacology, Addiction Science, and Toxicology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Insights
Embryonic hyperglycemia impairs retinal development, affecting synaptic ribbon maturity and potentially causing visual defects. This study highlights how high blood sugar during development disrupts crucial retinal connections.
Area of Science:
- Neuroscience
- Developmental Biology
- Ophthalmology
Background:
- Embryonic hyperglycemia adversely affects retinal development, causing visual behavior abnormalities and cellular deficits.
- Synaptic disorganization is a hallmark of neurological disorders, prompting investigation into its role in retinal development.
Purpose of the Study:
- To investigate the impact of embryonic hyperglycemia on the development of retinal ribbon synapses.
- To understand how hyperglycemia affects synaptic protein expression and localization in the developing retina.
Main Methods:
- Utilized reverse transcription quantitative PCR (RT-qPCR) to analyze synaptic protein transcription.
- Employed immunofluorescence labeling to examine synaptic protein localization in zebrafish embryos.
Main Results:
- Hyperglycemic zebrafish larvae exhibited compromised synaptic ribbon maturity.
- Altered expression of 'ribeye' was observed, correlating with delayed retinal ribbon synapse formation.
- An increase in immature synaptic ribbons was noted in hyperglycemic conditions.
Conclusions:
- Embryonic hyperglycemia disrupts retinal synapse development by interfering with synaptic ribbon maturation.
- These disruptions in synaptic development may lead to visual impairments.
- Zebrafish models offer a platform for further mechanistic studies of hyperglycemia's effects on retinal synapse development.
Abstract:
Embryonic hyperglycemia negatively impacts retinal development, leading to abnormal visual behavior, altered timing of retinal progenitor differentiation, decreased numbers of retinal ganglion cells and Müller glia, and vascular leakage. Because synaptic disorganization is a prominent feature of many neurological diseases, the goal of the current work was to study the potential impact of hyperglycemia on retinal ribbon synapses during embryonic development. Our approach utilized reverse transcription quantitative PCR (RT-qPCR) and immunofluorescence labeling to compare the transcription of synaptic proteins and their localization in hyperglycemic zebrafish embryos, respectively. Our data revealed that the maturity of synaptic ribbons was compromised in hyperglycemic zebrafish larvae, where altered ribeye expression coincided with the delay in establishing retinal ribbon synapses and an increase in the immature synaptic ribbons. Our results suggested that embryonic hyperglycemia disrupts retinal synapses by altering the development of the synaptic ribbon, which can lead to visual defects. Future studies using zebrafish models of hyperglycemia will allow us to study the underlying mechanisms of retinal synapse development.
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