The mechanism of 'forgetting' your fear

A glutamate receptor, the key neurotransmitter in the brain, plays an important role in the 'forget' process, researchers at the Salk Institute of Biological Studies said.

Their findings, published in the Journal of Neuroscience, can help scientists develop new therapies for many disorders, including phobias and anxiety disorders.

Stephen F. Heinemann, a doctoral professor at the Molecular Neuroscience Laboratory, who led the study, said: 'Most studies focus on the' learning 'process, but the' forget 'process (what has been learned) is also very important and understanding of this issue is very limited. Most people agree that being unable to 'forget' is a stress disorder after injury, and if we have a drug that can affect this gene, it can help soldiers return from war. 'forget' battle away fearful memories'.

Post-traumatic stress disorder or PTSD is an anxiety disorder that can develop after being exposed to a frightening event, or after bodily injuries. PTSD is affecting about 5.2 million Americans , according to the National Institutes of Health. 1 in 8 soldiers returned from the front with this disease.

But you don't need to be a soldier on the battlefield to develop this neurological disorder. Any frightening experience in everyday life can also form anxiety disorders. If the damaged memories persist, the emotional signals, sometimes unrecognizable, stimulate the repetition of memories that cause stress and fear.

To simulate anxiety disorders in humans, scientists train mice to fear a sound by attaching it to an electric shock in the leg. If this fear is continued by being exposed to the sound but without the above consequences, fear fades, a change in behavior called quenching fear, or learning alkalinity. processing.

Heinemann and his team are particularly interested in whether mGluR5, the metabotropic glutamate receptor 5, participates in some form of behavioral learning, has a role to play in controlling learning. Heinemann said: 'Controlling learning is thought to be a parallel learning mechanism that requires new information acquisition as well as restraining past experiences to be able to adapt to a new environment or situation'.

Picture 1 of The mechanism of 'forgetting' your fear Researchers found that a glutamate receptor plays an important role in the 'forget' process - this finding could help scientists develop new therapies for many disorders, including Obsessiveism, and anxiety disorders. (Photo: iStockphoto / Diane Diederich)

When the lead author, Dr. Jian Xu, put mice lacking genes for mGluR5, they could not eliminate the fear of completely harmless sounds. He said: 'You can train them to be afraid of sound, but they cannot erase the relationship between sound and previous negative experience.'

In the second series of experiments, Xu examined whether deleting mGluR5 affects the ability to learn spatial information. First he trained rats to find a platform hidden in a fixed position in the water maze. Although mutant mice took longer than normal mice to memorize the position of the underwater sink, after a few days the mutant mice were able to find the pedestal position equally quickly. normal mice.

Xu then moved the platform to another location in the water labyrinth and re-trained the animal. He observed that normal mice quickly changed their search strategy when they realized the platform had been moved to a new location. The mice lacking mGluR5 could not recognize that the pedestal was no longer there and kept coming back to the original position.

Xu explained: 'Mice without mGluR5 have very little ability to' forget 'what they have learned. We believe that the same mechanism is the cause of PTSD and mGluR can provide a potential target for therapeutic interventions'.

In addition to Xu and Heinemann, postdoctoral researcher Dr. Yongling Zhu, and Dr. Anis Contractor, also contributed to the study.

Refer:
Jian Xu, Yongling Zhu, Anis Contractor, and Stephen F. Heinemann.mGluR5 Has a Critical Role in Inhibitory Learning.Journal of Neuroscience, 2009;29 (12): 3676 DOI: 10.1523 / JNEUROSCI.5716-08.2009