Loss of protein changes axon to dendrite
By Ruth SoRelle, M.P.H.
The loss of a protein called ankyrin G by a neuron in the brain can change the character of the cell's components. In particular, its long, stringy axons that output information from the cell become more like the dendrites, which accept information.
That finding has important implications for brain and nerve injury as well as diseases that affect cognition, said Matthew N. Rasband, Ph.D., professor of neuroscience at Baylor College of Medicine, who published the results of his work with researchers at the University of Connecticut Health Center in Farmington in a recent report in the journal of Cell Biology.
Confused neuronal signals
"If the neuron gets confused, it does not know how to signal properly," said Rasband. "Ankyrin G is required for a neuron to maintain the distinction between an axon and a dendrite. This is the first time an axon has been converted into a dendrite in the laboratory." The opposite change – dendrite to axon – has been observed previously in models of nervous system injury.
Dendrites are rough multi-branched extensions from the neuron's cell body that are specialized to receive information. Most neurons have many dendrites but only one axon, a long thread of tissue that extends away from the cell body and only branches when it is far removed. It takes information away from the cell body and transmits it to other neurons or other organs.
Does this occur naturally?
One major question is whether this is just an interesting laboratory finding or if this axon-to dendrite change occurs after disease and injury?
"It's easy to imagine a scenario where an injury disrupts or damages ankyrin G," Rasband said. "The implication of this paper is that if it does occur, then the neuron would get confused and even though it was alive, not know where to send its signals."
He and his collaborators used viruses together with a relatively new technique called RNA interference or RNAi to reduce the amount of ankyrin G produced in a cell culture of neurons.
To study in models of disease
In the future, they plan to study the effects of the loss of ankryin G in models of diseases that affect the brain and nerves.
Other members of the Rasband laboratory who took part in this research are Kristian L. Hedstrom, now of the Yale University School of Medicine in New Haven, Conn. and and Yasuhiro Ogawa, now of Meiji Pharmaceutical University in Tokyo.
Funding for this work came from the National Institutes of health, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, Mission Connect and the National Multiple Sclerosis Society.
View an abstract of this article.
