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Updated: May 7, 2026
Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish
Published on: May 5, 2021
Macrophages warrant Mauthner cell axon regrowth by preventing late-stage hyperglycemia in zebrafish
Jing Bai1, Siting Lai1, Yubei Huang1
1School of Medicine, South China University of Technology , Guangzhou, Guangdong, People's Republic of China.
Abstract:
Axonal regeneration in the central nervous system is imperative for functional restoration following spinal cord injury (SCI). Myeloid cells are key regulators of axonal regeneration, yet their roles are not fully revealed. SCI perturbs glucose metabolism; however, its precise impact on axonal regeneration remains undefined. Moreover, whether myeloid cells orchestrate glucose metabolic responses to facilitate regeneration is unclear. Here, using the zebrafish Mauthner cell axon transection model, we demonstrate that following SCI, myeloid cell deficiency leads to a late-stage glucose surge, which leads to impaired axonal regeneration. We further identify glucagon signalling as a critical molecular determinant of this metabolic dysregulation and show that targeted mutations in gcga or its receptors (gcgra, gcgrb) rescue the axonal regeneration defects caused by myeloid cell deficiency. Finally, cell-depletion experiments demonstrated that macrophages are responsible for the late-stage hyperglycemia and defective axon regeneration of Mauthner cells. These findings suggest that glucose metabolism plays a critical role in macrophage-warranted axon regeneration in the spinal cord, positioning glucose homeostasis as a potential therapeutic target for enhancing axon regeneration and recovery.
Insights
Myeloid cell deficiency after spinal cord injury causes a glucose surge, impairing axon regeneration. Targeting glucagon signaling or macrophages may improve recovery.
Area of Science:
- Neuroscience
- Immunology
- Metabolism
Background:
- Axonal regeneration is crucial for recovery after spinal cord injury (SCI).
- Myeloid cells influence regeneration, but their metabolic roles are unclear.
- SCI disrupts glucose metabolism, impacting regeneration outcomes.
Purpose of the Study:
- To investigate the role of myeloid cells in regulating glucose metabolism post-SCI.
- To determine how glucose metabolism affects axonal regeneration.
- To identify molecular mechanisms linking myeloid cells, glucose, and regeneration.
Main Methods:
- Zebrafish Mauthner cell axon transection model.
- Myeloid cell depletion and macrophage depletion experiments.
- Genetic manipulation of glucagon signaling components (gcga, gcgra, gcgrb).
- Analysis of glucose levels and axonal regeneration.
Main Results:
- Myeloid cell deficiency caused late-stage hyperglycemia and impaired Mauthner cell axon regeneration.
- Glucagon signaling (gcga, gcgra, gcgrb) was identified as critical for this metabolic dysregulation.
- Targeting glucagon signaling or depleting macrophages rescued regeneration defects.
- Macrophages were identified as responsible for hyperglycemia and impaired regeneration.
Conclusions:
- Glucose metabolism is vital for macrophage-mediated axon regeneration in the central nervous system.
- Macrophage-controlled glucose homeostasis is essential for functional recovery after SCI.
- Modulating glucose metabolism presents a potential therapeutic strategy for SCI recovery.
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