Summary: New research has revealed that neurons act as “backup batteries” to maintain mental function under pressure of power stress. Researchers discovered that neurons can access glucose reserves when oxygen or mitochondrial function is slowed down by superior biosensors and worms.
This physiological versatility, or “glycogen-dependent oxidative plasticity,” demonstrates that neurons are more self-sufficient than originally thought. The finding may lead to novel therapies for neurological conditions where power loss is a key factor.
Important Information
- Contrary to popular belief, cells have their own power reserves.
- When there is little air or mitochondrial function, cells rely on glucose to adapt to stress.
- Findings may have the potential to develop treatments for injury, seizures, and aging.
Yale University
A new study from Yale University has discovered that neurons , — , the energy-hungry tissues that connect and control brain activity, are equipped with “backup batteries” that blow in to keep the mind operating during times of physiological tension.  ,
Experts describe how , neurons , store , their own glucose, a form of sugar, that helps , neurons , remain adaptable when their primary power sources fail, in the journal Proceedings of the National Academy of Sciences.
The findings provide new insights into neuron , neuron , cells , can , adapt their , digestion, and other areas of study that may influence treatments for neurological conditions like strokes, neurodegeneration, and epilepsy, all of which involve power failure.  ,
According to co-lead artist Milind Singh, a graduate student in cell biology at the Yale School of Medicine  ( YSM),” Traditionally, it was believed that glial cell served as “energy stores,” storing glucose and providing cells with energy as needed.  ,
” But we now know that neurons themselves can save carbohydrate and degrade it when the pressure is on. It’s like learning that your vehicle is a hybrid; it’s not just dependent on fuel stations; it’s been using an emergency power the entire time.
The research team used Caenorhabditis elegans ( C. elegans ), a microscopic roundworm known as Caenorhabditis elegans ( C. elegans ), a genetically encoded fluorescent biosensor called HYlight for the study, and a genetically encoded fluorescent biosensor that glows in response to changes in glycolysis, which is the process where cells use glucose for energy.  ,
Researchers  used specially designed equipment to accurately control the oxygen amount the existing worms experienced and monitor how neurons responded to power stress in real time.
The enzyme PYGL-1, the spider’s version of the animal glucose phosphorylase enzyme that converts glucose into neuronal fuel, was discovered by researchers as a breakthrough.
When PYGL-1 was removed by researchers, the insect neurons was no longer generate sufficient power during low-oxygen tension. When the enzyme was restored in neurons, the failure was reversed.
According to co-lead writer Aaron Wolfe, a postdoctoral researcher in doctoral neuroscience,” we discovered that neurons adapt to energy stress using two distinct strategies: one that is glycogen-dependent and the other that isn’t.”
When the mitochondria, one of the body’s primary energy producers, aren’t functioning properly, the glycogen-dependent pathway becomes especially crucial. In those circumstances, carbohydrate acts as a storage system to generate power via glycolysis.
The team came up with the term “glycogen-dependent glycolytic plasticity” ( GDGP ) to describe this phenotype. They discovered that GDGP is particularly crucial when mitochondrial function is compromised, such as when air is scarce, in ischemia.
In these circumstances, glycogen acts as a low-cost, quick-access fuel source, allowing neurons to function while various systems may stall. This physiological resilience, or “glycolytic plasticity,” helps neurons maintain their primary functions when under stress.
The brain’s traditional concept of how it fuels itself is challenged by our job. Cells are more self-sufficient than we thought, Singh said.
The study, co-author Daniel Colón-Ramos, professor of neuroscience and cell biology at YSM, stated that the research supports the idea that carbohydrate serves as an “energy capacitance” in neurons.  ,
This reserve is buffer fast shifts in electricity demand, Colón-Ramos said, just like in muscles.
” That flexibility may be important for how the brain maintains function and how it responds to stress,” he said. This study reshapes our understanding of brain power digestion and opens new avenues for research on how to protect and support cerebral work in disorder.
Other notable authors from Yale include Richard Goodman, a  research scientist in neuroscience, Sarah Emerson, a postdoctoral researcher in neuroscience, Ian J. Gonzalez, a graduate student in cell biology, and Anjali A. Vishwanath and Anastasia Tsives, post-doctoral researchers in neuroscience.
About this news from neuroscience research
Author: Bess Connolly
Source: Yale
Contact: Bess Connolly – Yale
Image: The image is credited to Neuroscience News
Original research: Free of charge.
Milind Singh et al.,” Glycogen helps neurons develop glycolytic plasticity..” PNAS
Abstract
Glycogen helps neurons develop glycolytic plasticity.
Although glycogen has the largest energy reserve in the brain, it is not well understood how it affects in vivo neuronal energy metabolism.
We created a system in Caenorhabditis elegans to dynamically monitor glycolytic states in single cells of living animals using the glycolytic sensor HYlight, and demonstrated that neurons can dynamically regulate glycolysis in response to activity or transient hypoxia.
We discovered that neurons require PYGL-1, an ortholog of the human glycogen phosphorylase, for glycolytic plasticity after performing an RNAi screen.
We identified two glycolytic plasticity mechanisms in neurons: glycogen-dependent glycolytic plasticity ( GDGP ) and glycogen-independent glycolytic plasticity ( GDGP ). We discover that GDGP is used in mitochondrial function mutants or in transient hypoxia-causing conditions.
We discover that the loss of GDGP affects glycolytic plasticity and causes synaptic vesicle recycling issues during hypoxia.
Our study together demonstrates that neurons can directly use glycogen as a fuel source in vivo to maintain glycolytic plasticity and synaptic function.
