Mobilizing Mitochondria May Be Key to Regenerating Damaged Neurons: Mouse Study

Summary: A new study reports boosting the transport of mitochondria along axons enhances the ability for mouse nerve cells to replace themselves following injury.

Source: Rockefeller University Press.

Researchers at the National Institute of Neurological Disorders and Stroke have discovered that boosting the transport of mitochondria along neuronal axons enhances the ability of mouse nerve cells to repair themselves after injury. The study, “Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits,” which has been published in The Journal of Cell Biology, suggests potential new strategies to stimulate the regrowth of human neurons damaged by injury or disease.

Neurons need large amounts of energy to extend their axons long distances through the body. This energy – in the form of adenosine triphosphate (ATP) – is provided by mitochondria, the cell’s internal power plants. During development, mitochondria are transported up and down growing axons to generate ATP wherever it is needed. In adults, however, mitochondria become less mobile as mature neurons produce a protein called syntaphilin that anchors the mitochondria in place. Zu-Hang Sheng and colleagues at the National Institute of Neurological Disorders and Stroke wondered whether this decrease in mitochondrial transport might explain why adult neurons are typically unable to regrow after injury.

image shows axons

Sheng and his research fellow Bing Zhou, the first author of the study, initially found that when mature mouse axons are severed, nearby mitochondria are damaged and become unable to provide sufficient ATP to support injured nerve regeneration. However, when the researchers genetically removed syntaphilin from the nerve cells, mitochondrial transport was enhanced, allowing the damaged mitochondria to be replaced by healthy mitochondria capable of producing ATP. Syntaphilin-deficient mature neurons therefore regained the ability to regrow after injury, just like young neurons, and removing syntaphilin from adult mice facilitated the regeneration of their sciatic nerves after injury.

“Our in vivo and in vitro studies suggest that activating an intrinsic growth program requires the coordinated modulation of mitochondrial transport and recovery of energy deficits. Such combined approaches may represent a valid therapeutic strategy to facilitate regeneration in the central and peripheral nervous systems after injury or disease,” Sheng says.

ABOUT THIS NEUROLOGY RESEARCH ARTICLE

Funding: This research was supported by National Institutes of Health, NIH/National Institute of Neurological Disorders and Stroke.

Source: Ben Short – Rockefeller University Press
Image Source: This NeuroscienceNews.com image is credited to Zhou et al., 2016.
Original Research: Abstract for “Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits” by Bing Zhou, Panpan Yu, Mei-Yao Lin, Tao Sun, Yanmin Chen, and Zu-Hang Sheng in Journal of Cell Biology. Published online June 7 2016 doi:10.1083/jcb.201605101

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Rockefeller University Press. “Mobilizing Mitochondria May Be Key to Regenerating Damaged Neurons: Mouse Study.” NeuroscienceNews. NeuroscienceNews, 7 June 2016.
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Abstract

Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits

Although neuronal regeneration is a highly energy-demanding process, axonal mitochondrial transport progressively declines with maturation. Mature neurons typically fail to regenerate after injury, thus raising a fundamental question as to whether mitochondrial transport is necessary to meet enhanced metabolic requirements during regeneration. Here, we reveal that reduced mitochondrial motility and energy deficits in injured axons are intrinsic mechanisms controlling regrowth in mature neurons. Axotomy induces acute mitochondrial depolarization and ATP depletion in injured axons. Thus, mature neuron-associated increases in mitochondria-anchoring protein syntaphilin (SNPH) and decreases in mitochondrial transport cause local energy deficits. Strikingly, enhancing mitochondrial transport via genetic manipulation facilitates regenerative capacity by replenishing healthy mitochondria in injured axons, thereby rescuing energy deficits. An in vivo sciatic nerve crush study further shows that enhanced mitochondrial transport in snph knockout mice accelerates axon regeneration. Understanding deficits in mitochondrial trafficking and energy supply in injured axons of mature neurons benefits development of new strategies to stimulate axon regeneration.

“Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits” by Bing Zhou, Panpan Yu, Mei-Yao Lin, Tao Sun, Yanmin Chen, and Zu-Hang Sheng in Journal of Cell Biology. Published online June 7 2016 doi:10.1083/jcb.201605101

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connie dello buono

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