The genetic conquest of fear

The genetic conquest of fear

The conquest of fear seems to be drawing near. In a recent spate of experiments conducted on mice, scientists have discovered that the elimination of a specific gene called stathmin can raise courage levels and make the animals more daring in their environment.

Stathmin, the gene of fear, is the protein inhabiting a certain brain area called amygdala, which is activated highly in humans and other mammals when they are fearful and anxious. This pioneering study has credibly established link between stathmin (or oncoprotein 18) and fear conditioning.

This new information, published in the scientific journal called 'Cell', has the potential to open up novel therapeutic methods to cure and combat anxiety related disorders in human beings. The brain functioning of all mammals is mostly similar and the experiments showed that removing the gene did not negatively affect other kinds of development in the mice. The applications can range from production of new medicines to physiological treatments of trauma and general anxiety.

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Gleb Shumyatsky, from Rutgers, and Dr. Eric Kandel from the Howard Hughes Medical Institute Center for Neurobiology and Behavior, spearheaded the path breaking research with an assorted team from their respective institutes and Harvard and the Albert Einstein College of Medicine. The experiments compared the behavior of two groups of mice, one with the gene and the other without it.

They discovered that stathmin is normally responsible for a chain of cell disintegration and regrowth, which in turn leads to neuro-biological messaging and learning, which further contributes to memory build-up. When fear is experienced from a certain stimulus, the learning and memorizing of that emotion fear happens in the brain due to stathmin. Scientists found the process lacking or insufficient in mice without stathmin, ridding their brains of the ability to learn fear or depend on instinctive fear in anxious circumstances. Moreover, they began exhibiting behavior deviating from normal. For instance, generally mice are cautious of open areas, but in non-stathmin mice, no such fear was displayed as they moved around with ease in open areas. Contrarily, the normal group attempted to hide from such open passages.

However, the stathmin deficient mice were equally responsive to pain stimuli as the normal group, and as skilled at spatial judgments as well.

The study throws up implications for both learned and instinctive fear. Learned fear is a result of conditioning and hence involves memory. Memories are created in and stay in the amygdala.

This new scientific discovery promises a lot. It will help to evolve means to combat a gamut of human psychological malfunctioning such as phobia, borderline personality disorder, shock trauma, stage fear, stress and anxiety. It will definitely impart gainful insights into the process of how fear is felt and memorized. Additionally and most significantly, it will lead to further research on new medicinal therapy for those paralyzed with fear.