The Migration of Sensory Neurons Following Chemical-Genetic B-Cell Ablation in Danio reno Larvae
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Date
2018
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Biological Sciences
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Abstract
Peripheral nerves act as a vital bridge between the environment and the brain; environmental information is received by sensory neurons and transported, through electrical impulses, along axons to the central nervous system (CNS). The brain processes the information and sends a response back to target organs or muscles through motor axons. When any component of the peripheral nerve is damaged a condition called peripheral neuropathy can develop. This condition often presents in the form of numbness, aching, and burning in the extremities as a result of the nerve damage. One specific cause of peripheral neuropathy is hyperglycemia, an excess of blood glucose which is often associated with diabetes. Damage may be present in both the sensory and motor nerves that make up the peripheral nervous system (PNS), diminishing the ability of those affected to interact with their environment. Preliminary data from the Clark lab suggests that sensory neurons migrate away from their origins at the dorsal root ganglia (DRG). Based upon this work and the knowledge that nerve changes occur in correspondence to hyperglycemia, I hypothesize that the onset of hyperglycemia by pancreatic B-cell ablation results in peripheral neuropathy. Future work will include a small molecule drug screen that may be able to provide insight on the molecular mechanisms underlying hyperglycemia-induced degeneration of the peripheral nerve. Additionally, I plan to study how hyperglycemia presents in the CNS utilizing the same model system.