Fudan University Research proposes a new strategy to eliminate fear memory
December 12, 2016 Source: Science Network
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];When it comes to "fear," people will inevitably "color change." In particular, the fear of suffering from trauma is like a "time bomb". I don't know when it will "pick up the heartstrings." In order to solve the "chain reaction" caused by fear, we have adopted a comprehensive strategy of psychological intervention and drug treatment to restrain the "rebound" of fear. However, once the persistence of psychological intervention and drug treatment is interrupted, the original fear will once again come to mind.
This problem caused the thinking and experimental exploration of the research team of Yan Yongchun, a researcher at the Institute of Brain Science, Fudan University. Their experiments showed that transplanting embryonic brain-inhibiting neural precursor cells into the amygdala of adult animals can effectively suppress the "regrowth" of fear memory, suggesting that a new strategy can be adopted to eliminate fear memory.
At 1 am on December 9, relevant research results were published online in the journal Neuron. It is reported that the research was funded by the Ministry of Science and Technology 973 project, the National Natural Science Foundation of China, and the Fund's major research project cultivation project, and was completed by Yan Yongchun and the graduate students of the research group, Yang Wuzhou and Liu Tingting.
Double-edged sword: fear has both protective effects and can cause serious mental illness
Fear, a high-level psychological emotion, is a struggle after being struggling in the face of danger and being frightened. Fear emotions give life individuals the ability to adapt in different environments, and the fears generated by dangers have a protective effect on animals to stimulate their potential and enhance their ability to survive.
However, the existence of anything has two sides. The fear generated after a heavy blow is lurking in the brain, leaving indelible traumatic memories in the brain. Once stimulated by foreign objects, it can cause intense mental illness (ie, post-traumatic stress syndrome, Post-traumatic Stress Disorder, PTSD). Patients often show strong anxiety and depression with symptoms such as chronic pain, cardiovascular disease, metabolic syndrome, and drug abuse (such as drugs, tobacco, and alcohol dependence). According to statistics, 80% of adults have experienced at least one traumatic event in their lifetime, and 5-10% of them have severe psychological trauma and can be diagnosed as PTSD patients.
A comeback: PTSD treatment encounters bottleneck
When negative fear memory is derived from traumatic mental illness, symptoms are often relieved through psychological intervention and medication. For example, in a PTSD patient after a car accident, the psychiatrist will let the patient watch some car accident scenes to convey the message that the scene is harmless, so that the patient can overcome the fear and calmly recall the situation at that time. At the same time, the doctor will relieve the emotion according to the patient's manifestation or anxiety or depression.
However, the effects of these two therapies are not significant. Once the treatment is stopped, the negative fear memory may be evoked again, and the mental symptoms “returnâ€. How to suppress the awakening of fear memory has become an important issue in brain science research.
Young adult amygdala: a new strategy for PTSD treatment
The new thinking of the Yong Yongchun team comes from the full understanding of the brain's excitement, inhibition of the balance process and brain plasticity. There are two types of neurons in the cerebral cortex, excitatory neurons and inhibitory neurons. The former promotes the excitability of the human brain, while the latter inhibits the former. The balance of excitement and inhibition ensures the normal activity of the brain. The nucleus of the brain, the amygdala, is a key part of dealing with fear information and generating fear memory. After intense stimulation, the amygdala is highly excited, destroying the normal balance of excitement-suppression, which is the source of fear memory. If the inhibition process is enhanced, is it beneficial to the decline of fear memory?
On the other hand, as it develops, the plasticity of the amygdala gradually subsides. There is experimental evidence that the younger the animal, the stronger the plasticity of the brain, and the more likely the negative fear memory to subside. If the mature amygdala is “rejuvenatedâ€, will it accelerate the decline of fear memory?
Based on the above analysis, the team believes that if embryonic inhibitory neurons are transplanted into the highly excited adult amygdala, it can inhibit the excessive excitability of the amygdala and possibly “young†the adult amygdala. Awakening of fear memory.
Sleeping fear memory: neuronal transplantation enhances synaptic plasticity
The Yong Yongchun team used mice as experimental subjects to transplant the medial ganglionic eminence (MGE)-derived inhibitory neurons into the bilateral amygdala region of adult mice. The researchers combined the sound with the electric stimulation of the foot to give the mouse a strong fear of memory, that is, whenever the sound is heard, it produces a fear reaction—long-term “stiffnessâ€. Thereafter, the mice were given fear-eliminating training (only the mouse was given a sound without applying plantar stimulation) to suppress fear memory.
The results of the study showed that the fear-elimination training after transplantation of inhibitory neurons can permanently suppress the spontaneous recovery of fear memory and the reawakening of fear memory. Interestingly, the Yong Yongchun team found that only transplanting young, incompletely mature inhibitory neurons can effectively promote the regression of negative fear memory.
Further, the Yong Yongchun team confirmed through experiments that the inhibitory neural progenitor cells formed extensive synaptic connections with host neurons two weeks after amygdala transplantation. At the same time, it was found that compared with transplanted mature neurons, transplanting young neurons not only regulates the amygdala excitation and inhibition balance, but also enhances the synaptic plasticity of the host neural circuit. More importantly, the researchers confirmed that transplanted young neurons can change the adult amygdala synaptic plasticity level from an adult state to a young state, so that the regressive negative fear memory is not easily re-evoked.
At present, the ability of mice to produce fear after embryonic inhibitory neuronal transplantation has not been affected. Yan Yongchun said: "Selectively deleting fear memory with negative effects is beneficial to the health of the brain." At the same time, Yan Yongchun also pointed out: "The study is only in the stage of animal experiment, and it is really used in clinical treatment. There is a long way to go."
This study demonstrates that transplantation of young inhibitory neurons can rejuvenate the adult host amygdala, thereby making the host amygdala more malleable, making it easier for mice that have acquired fear memory to suppress fear through fear elimination training. Awakening of memory. Experts believe that this study is not only important for understanding the amygdala fear memory loop, but also provides a new strategy and ideas for the treatment of post-traumatic stress syndrome.
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