Sensory deprivation reduces new cell size in the olfactory system

Main Category: Public Health
Article Date: 07 Apr 2005 - 12:00 PDT

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Sensory deprivation causes changes in new cell size and excitability in the olfactory system, which governs the ability to smell, according to a study in Neuron by a Yale School of Medicine researcher.

"This gives new insight into how stem cells in the olfactory system may be used to restore function in a brain that has been compromised by degenerative disease or trauma," said Gordon Shepherd, M.D., co-author of the paper and professor of neuroscience at Yale.

Shepherd, on sabbatical with Pierre-Marie Lledo of the Pasteur Institute, investigated how the olfactory system responds to changes brought about by injury or different levels of activity. They closed one nostril in mice, a common sensory deprivation procedure, and then observed how the olfactory system adjusted to the change in sensory input.

The olfactory system is one of the most plastic regions of the brain, with nerve cells that are continually replenished by stem cells. Stem cells in the nose replenish the sensory cells, which send the odor messages to the olfactory bulb. "There also are stem cells deep in the brain that replenish the interneurons, which carry out much of the processing of the odor messages that takes place in the olfactory bulb," Shepherd said.

When deprived of sensory input, there was a reduction in the size of the new interneurons, but this was compensated by an increase in their excitability. Shepherd and colleague Michele Migliore, visiting scientist from Palermo, Sicily, carried out simulations which showed how these two changes balance each other. "This preserves the function of the interneurons in being able to process input if it were to be restored," Shepherd said.

In another recent study, Shepherd and Migliore extended their model to show how processing takes place within the olfactory networks. The new data on plasticity will be incorporated into the new model.

In addition to Shepherd and Migliore, co-authors included Armen Saghatelyan, Pascal Roux, Christelle Rochefort, David Desmaisons and Pierre Charneau of the Pasteur Institute.

Neuron 46: 103-116 (April 7, 2005)

Contact: Jacqueline Weaver
jacqueline.weaver@yale.edu
203-432-8555
Yale University
http://www.yale.edu