PUBLICATION
            Regenerative potential and limitations in a zebrafish model of hyperglycemia-induced nerve degeneration
- Authors
- Sargent, S., Brennan, A., Clark, J.K.
- ID
- ZDB-PUB-230308-32
- Date
- 2023
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 252(6): 742-760 (Journal)
- Registered Authors
- Keywords
- hyperglycemia, perineurial glia, perineurium, peripheral nerve, regeneration, vertebral development
- MeSH Terms
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                - Zebrafish*
- Animals
- Hyperglycemia*/chemically induced
- Nerve Degeneration
- Peripheral Nervous System
- Mammals
 
- PubMed
- 36879394 Full text @ Dev. Dyn.
            Citation
        
        
            Sargent, S., Brennan, A., Clark, J.K. (2023) Regenerative potential and limitations in a zebrafish model of hyperglycemia-induced nerve degeneration. Developmental Dynamics : an official publication of the American Association of Anatomists. 252(6):742-760.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
Background Previous work from our lab has described a model of motor nerve degeneration in hyperglycemic zebrafish larvae which resembles mammalian models of diabetic peripheral neuropathy (DPN). Here, we optimized the hyperglycemic-induction protocol, characterized deficits in nerve structure and behavioral function, and then examined the regenerative potential following recovery from the hyperglycemic state.
Results In agreement with our previous work, hyperglycemia induced motor nerve degeneration and behavioral deficits. However, the optimized protocol initiated disruption of tight junctions within the blood-nerve barrier, a phenotype apparent in mammalian models of DPN. Following a ten-day recovery period, regeneration of motor nerve components was apparent, but behavioral deficits persisted. We next examined the effect of hyperglycemia on the musculoskeletal system and found subtle deficits in muscle that resolved following recovery, and robust deficits in the skeletal system which persisted following recovery.
Conclusion Here we optimized our previous model of hyperglycemia-induced motor nerve degeneration to more closely align with that observed in mammalian models and then characterized the regenerative potential following recovery from hyperglycemia. Notably, we observed striking impairments to skeletal development, which underscores the global impact hyperglycemia has across systems, and provides a framework for elucidating molecular mechanisms responsible for regenerative events moving forward.
            
    
                
                    
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