To investigate stathmin's role in more detail, the researchers created mice lacking that gene, and examined the brain activity in the lateral nucleus of their amygdalas. Recent work from other labs had shown that during fear learning, the connections between the neurons in this part of the brain strengthen. In stathmin-deficient mice, however, the connections between these neurons remained virtually unchanged, despite repeated stimulation.
These results were good indications that stathmin might play a role in learned fear. To determine whether a lack of stathmin actually altered animals' behavior in situations likely to trigger fear, the scientists used several standard laboratory tests. Mice were trained to associate an electric shock with either an auditory tone or a particular location in a cage. After the training period, normal mice would freeze when they encountered the tone or location that they'd learned was likely to accompany a shock. Stathmin-deficient mice, on the other hand, seemed unnerved by those stimuli, carrying on their normal activities boldly, without fear.
From these experiments, it was clear to the scientists that stathmin was needed for fear learning. To find out whether it might also contributed to innate fear, the scientists took advantage of mice's natural fear of open spaces. Unlike normal mice, which cower on the edges of an open field and stay near the center of a plus-shaped maze, mice without stathmin were much more adventurous, readily exploring exposed areas.
The authors concluded from their experiments that stathmin is required for both innate and learned fear.
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Contact: Jennifer Michalowski
michalow@hhmi.org
301-215-8576
Howard Hughes Medical Institute
18-Nov-2005