We all remember September 11, 2001, only too well; this is because our brain etches fearful memories deep into our system. This property can provide selection advantages to creatures that can learn to avoid fearful situations and improve their chances to survive in a dangerous world. However, the intensification of fearful memories sometimes charges a high toll. Patients with Post-Traumatic Stress Disorder, for example, can never forget the traumatic experience they went through. Just hearing a bus horn may throw them back into the battle they wish to forget, and they will freeze in response and loose contact with their surroundings. It is clearly of much significance to unravel the genes and proteins that are responsible for such responses; once this is achieved, the door will be opened for developing rationally designed therapeutic treatments for down tuning the fierce impact of traumatic memories.
With these goals in mind, a joint team of researchers at the Max Planck Institute for Experimental Medicine in Gottingen, Germany and at The Hebrew University of Jerusalem in Israel explored memory processes in mice following immobilization stress. In their learning and memory model, mice learn to associate a fearful event with its context. Immobilization stress before subjecting mice to the learning paradigm will let the mice remember this context better; once they are back in the fearful environment, they stop moving, they "freeze". In parallel, stress leads to a change in brain neurons' gene expression. One specific change involves the acetylcholinesterase gene, which normally produces a protein product that adheres to synapses (the interaction sites through which nerve cells communicate with each other). Following stress, the same gene produces large quantities of a secretory protein with modified properties.
The effects of the observed changes in gene functioning were also tested. This involved measuring neuronal electrical signals. In the current sPage: 1 2 Related biology news :1
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