Given all the research showing the importance of sleep for consolidating memories, it should come as no great surprise that the reverse is also true: depriving yourself of sleep could help you forget experiences you would prefer not to remember.
In the study, 28 student volunteers were shown 14 short video clips, half of which showed safe driving down a city street, and half showed the car being involved in a nasty crash. Half of the volunteers were then deprived of sleep while the other half received a normal night's sleep. The next day, they were shown pictures and asked to indicate whether they had appeared in the clips they had seen. They were also asked to rate the fear evoked by the image, and their physiological responses measured. They were tested again 3 and 10 days later.
While there was no difference between the two groups in picture recognition, the control group rated the images from the crash videos as fearful, and these responses generalized over time to the other images. However, those who were sleep deprived showed such reactions only on the first day.
The finding suggests a possible therapy for PTSD or other anxiety disorders.
 . Sleep Deprivation Facilitates Extinction of Implicit Fear Generalization and Physiological Response to Fear. Biological Psychiatry [Internet]. 2010 ;68(11):991 - 998. Available from: http://www.sciencedirect.com/science/article/B6T4S-51509J0-4/2/311b47a7c36c915b545c8422d8489966
A mouse study has revealed the brain becomes overly stimulated after a traumatic event causes an ongoing, frenzied interaction between two brain proteins long after they should have disengaged. However, the injection of newly developed drugs into the hippocampus within a five hour window calmed this process, and prevented the development of a post-traumatic fear response.
The new research shows the potential for PTSD occurs when a stressful event causes a flood of glutamate, which then interacts with a second protein (Homer1a). This protein continues to stimulate metabotropic glutamate receptor 5 [mGluR5] after the glutamate has dissipated. The new drugs bind mGluR5 and reverse its activity.
 . Metabotropic Glutamate Receptor 5/Homer Interactions Underlie Stress Effects on Fear. Biological Psychiatry [Internet]. 2010 ;68(11):1007 - 1015. Available from: http://www.sciencedirect.com/science/article/B6T4S-51FPJ9X-9/2/951f58a15b0f6f5269091c17cc2e035e
Older news items (pre-2010) brought over from the old website
Scent of fear impacts cognitive performance
A study involving 75 female students found that those who were exposed to chemicals from fear-induced sweat performed more accurately on word-association tasks than did women exposed to chemicals from other types of sweat or no sweat at all. When processing meaningfully related word pairs, the participants exposed to the fear chemicals were significantly more accurate than those in either the neutral sweat or the control (no-sweat) condition. When processing word pairs that were ambiguous in threat content, such as one neutral word paired with a threatening word or a pair of neutral words, subjects in the fear condition were significantly slower in responding than those in the neutral sweat condition.
Chen, D., Katdare, A. & Lucas, N. 2006. Chemosignals of Fear Enhance Cognitive Performance in Humans. Chemical Senses, Advance Access published on March 9, 2006
Memory of fear more complex than supposed
It seems that fear memory is more complex than has been thought. A new mouse study has shown that not only the hippocampus and amygdala are involved, but that the prefrontal cortex is also critical. The development of the fear association doesn’t occur immediately after a distressing event, but develops over time. The process, it now seems, depends directly on a protein called NR2B.
 . Roles of NMDA NR2B Subtype Receptor in Prefrontal Long-Term Potentiation and Contextual Fear Memory. Neuron [Internet]. 2005 ;47(6):859 - 872. Available from: http://www.cell.com/neuron/abstract/S0896-6273(05)00689-6
How trauma triggers long-lasting memories in the brain
A rat study sheds more light on why emotional experiences tend to be better remembered than emotionally neutral events. The study found that emotionally arousing events activated the amygdala, which then increased a specific protein — activity-regulated cytoskeletal protein ("Arc") — in the neurons in the hippocampus. It's thought that Arc helps store these memories by strengthening the synapses.
 . Memory-influencing intra-basolateral amygdala drug infusions modulate expression of Arc protein in the hippocampus. Proceedings of the National Academy of Sciences of the United States of America [Internet]. 2005 ;102(30):10718 - 10723. Available from: http://www.pnas.org/content/102/30/10718.abstract
Why traumatic memories have the power they do
In the first imaging study to look at retrieval of emotional memories after a long period (one year after encoding), researchers found that people did recall emotional images, both pleasant and unpleasant, better than emotionally-neutral images. This recall was associated with higher activity in both the amygdala and the hippocampus. The synchronicity of activity between these two regions suggested that each region triggers the other, creating a self-reinforcing "memory loop" in which an emotional cue might trigger recall of the event, which then loops back to a re-experiencing of the emotion of the event. The findings suggest why people subject to traumatic events may be trapped in a cycle of emotion and recall that aggravates post-traumatic stress disorder, and may also suggest why therapies in which people relive such memories and reshape perspective to make it less traumatic can help people cope with such memories.
 . Remembering one year later: Role of the amygdala and the medial temporal lobe memory system in retrieving emotional memories. Proceedings of the National Academy of Sciences of the United States of America [Internet]. 2005 ;102(7):2626 - 2631. Available from: http://www.pnas.org/content/102/7/2626.abstract
Reducing the trauma of traumatic memories
For some, stressful memories can reawaken intense fear, with undesirable consequences. A new study involving mice has found that such stress induces a change in the expression of the acetylcholinesterase gene, which normally produces a vital protein that adheres to neuronal synapses. Following stress, however, the same gene produces large quantities of a protein with modified properties that results in heightened electrical signals in the nerve cells communicating through these synapses. The effect is to create reactions of extreme fright or immobilizing shock. Later encounter with a context which triggers those stressful memories can set off that same neuronal reaction. The researchers have developed an "antisense" agent that acts to neutralize the process whereby the modified protein is produced, thereby preventing the extreme reaction.
 Stress-induced alternative splicing of acetylcholinesterase results in enhanced fear memory and long-term potentiation. Mol Psychiatry [Internet]. 2003 ;9(2):174 - 183. Available from: http://dx.doi.org/10.1038/sj.mp.4001446