PUBLICATION
Disruption of peripheral nerve development in a zebrafish model of hyperglycemia
- Authors
- Ennerfelt, H., Voithofer, G., Tibbo, M., Miller, D., Warfield, R., Allen, S., Kennett Clark, J.
- ID
- ZDB-PUB-190704-11
- Date
- 2019
- Source
- Journal of neurophysiology 122(2): 862-871 (Journal)
- Registered Authors
- Keywords
- hyperglycemia, motor nerve, myelination, perineurial glia, sensory neuron
- MeSH Terms
-
- Axons*/metabolism
- Axons*/pathology
- Zebrafish
- Behavior, Animal/physiology
- Diabetic Neuropathies*/etiology
- Diabetic Neuropathies*/metabolism
- Diabetic Neuropathies*/pathology
- Larva
- Animals
- Disease Models, Animal
- Peripheral Nerves*/metabolism
- Peripheral Nerves*/pathology
- Sensory Receptor Cells*/metabolism
- Sensory Receptor Cells*/pathology
- Hyperglycemia/chemically induced
- Hyperglycemia/complications*
- PubMed
- 31268813 Full text @ J. Neurophysiol.
Citation
Ennerfelt, H., Voithofer, G., Tibbo, M., Miller, D., Warfield, R., Allen, S., Kennett Clark, J. (2019) Disruption of peripheral nerve development in a zebrafish model of hyperglycemia. Journal of neurophysiology. 122(2):862-871.
Abstract
Diabetes mellitus-induced hyperglycemia is associated with a number of pathologies such as retinopathy, nephropathy, delayed wound healing and diabetic peripheral neuropathy (DPN). Approximately 50% of patients with diabetes mellitus will develop DPN, which is characterized by disrupted sensory and/or motor functioning, with treatment limited to pain management. Zebrafish (Danio Rerio) are an emerging animal model used to study a number of metabolic disorders, including diabetes. Diabetic retinopathy, nephropathy, and delayed wound healing have all been demonstrated in zebrafish. Recently, our lab has demonstrated that following the ablation of the insulin producing β-cells of the pancreas (and subsequent hyperglycemia), the peripheral nerves begin to show signs of dysregulation. Here, we take a different approach, taking advantage of the transdermal absorption abilities of zebrafish larvae to extend the period of hyperglycemia. Following 5 days of 60mM D-glucose treatment, we observed motor axon defasciculation, disturbances in perineurial glia sheath formation, decreased myelination of motor axons, and sensory neuron mislocalization. This study extends our understanding of the structural changes of the peripheral nerve following induction of hyperglycemia, and does so in an animal model capable of potential DPN drug discovery in the future.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping