Research Profiles

 

 

 

 

 

 

 

 

 

RESEARCH PROFILES


Enteric Neurotransplantation


By Anita Kaiser
Canadian Spinal Research Organization

There are two main sites of neurological damage that occur after spinal cord injury:

  1. AXONS - long nerve cell processes that run up and down the spinal cord carrying motor and sensory information between nerve cells.

  2. NEURONS - nerve cells that carry and process information over short distances in the spinal cord.

These processes have the potential to regenerate but don't normally do so because inhibitors in the spinal cord present an inhospitable growth environment. The result is loss of function below the injury. One way of attempting to overcome neurological damage is by transplanting enteric neurons from the intestine to the injury site. The intestinal nervous system is similar to the central nervous system (CNS) . Enteric neurons are able to express a wide range of neurotransmitters, available in abundance, and do not cause host rejection since they are grafted back into the same individual. The transplanted nerve cells might connect with damaged cells to form connections across the region of injury, or they may directly replace cells lost through injury.


Another approach is the transplantation of enteric glia at the site of injury. These cells are similar to CNS astrocytes. They are supporting cells in the nervous system that function to ensheath axons and provide trophic factors which stimulate the growth and survival of neurons to extend and contact other nerve cells. After transplantation, the glia migrate up and down the spinal cord making paths for regenerating nerve cell processes to follow. The glia also help in preventing further tissue degeneration at the injury site.

VIDEO Dr. Michel Rathbone talks about Enteric Neurotransplantation. 

The ability of the glia to release trophic factors is triggered by messages sent from chemicals called PURINES. They make up part of the basic components of DNA and RNA. After an injury, all cells release large quantities of purines which help to protect from further damage to other neurons. The purines also cause the glia to release trophic factors to aid in repair. Often, the purine levels are insufficient in producing any significant changes so a synthetic purine has been created to supplement those naturally occurring. Currently, the effectiveness of the synthetic purine and its mechanism of action are being determined.

 


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