For more than a century, researchers have been working to understand the encoding, integration and awakening of memory. About 10 years ago, the mainstream view was that forgetting was a passive process in which unused memories decayed over time. But then some memory scientists began to encounter discoveries that seemed to contradict this hypothesis, and some began to suggest that the brain was a radical idea for forgetting.
Some animal experiments have confirmed this point: memory loss is not a passive process. Canadian scientists have found that the strength of connections between neurons depends on the number of structures called AMPA receptors that maintain the integrity of memory. But these receptors are not stable, they are constantly moved in and out of synapses. Scientists speculate that AMPA receptors can also be removed, suggesting that forgetting is an active process. If so, the AMPA receptor is not removed to prevent forgetting. Scientists blocked the removal of AMPA receptors in the hippocampus of rats, and as expected, the rats did not forget where the object was. In order to forget something, the rat brain seems to have to actively destroy synaptic connections.
Another group of scientists, in studying new neurogenesis (neurogenesis) in adult mice, found that increasing neurogenesis did not improve animal memory, but made rats forget more. This suggests that when neurons are integrated into the adult hippocampus, they are integrated into an existing, established circuit. If information has been stored in these loops and then rewired, it will be more difficult to obtain it. The hippocampus is not the place where long-term memory is stored. Allowing new information to cover old information can help animals learn to adapt to new environments. These experiments led scientists to conclude that forgetting is a function of memory.
There are two collisions of views on the mechanism behind active forgetting
If forgetting is a function of memory and an active behavior, when will our brain actively forget?
When we sleep, we also clear away memory and make some memories disappear. Xue Rong, a member of the Society of Neurology of the Chinese Medical Association and chief physician of Neurology of the General Hospital of Tianjin Medical University, said that what people experience when they are awake will be stored in the form of memory. However, not all experiences are worth remembering. These experiences were screened and classified according to their importance, and then two fates of memory consolidation and forgetting came into being. Through the monitoring of human sleep, there are also some views that can be confirmed that people will actively forget in sleep.
At present, there are two main opinions about the initiation of forgetting mechanism in sleep. One is probably related to hypothalamic melanin aggregation hormone neurons. Japanese scholars have found that a class of neurons activated only in REM phase (REM phase) can secrete a substance called melanin aggregation hormone, which can be mapped to the hippocampus, a brain region that is very important for learning and memory. Activation of melanin aggregation hormone neurons promotes sleep in REM phase and significantly inhibits the activity of hippocampal neurons, leading to forgetting. Animal experiments also confirm the validity of this theory. In the experiment, only in REM phase inhibited the melanocyte aggregation hormone cells which should have been activated in mice, and the memory of mice became better after awakening.
Another view may be related to synaptic reorganization to achieve synaptic homeostasis. It was found that after a certain period of awakening, the number of synapses, the volume of synapses and the number of receptors on membranes increased. These changes would lead to further occupying limited space, consuming energy and reducing the efficiency of synaptic transmission. Sleep can remove the increased receptors on the cell membrane during awakening and reduce a part of the new synapses that are not important. At the same time, it can also skillfully strengthen and preserve a small part of the more important synapses, restore the weight of synapses, ensure the synaptic homeostasis, and thus improve the efficiency of synaptic transmission.
Xue Rong indicated that the mechanism of forgetting may be related to synaptic reorganization to achieve synaptic homeostasis or hypothalamic melanin aggregation hormone neurons, but we still need to further study.
In addition, scientists believe that the brains forgetfulness may prevent an over-fitting effect. In the field of artificial intelligence, this over-fitting effect is defined as that when a mathematical model is too good at matching the data it uses to program, it cannot predict the data that may follow. For example, when a person is attacked by a dog, it is difficult to sum up experience and prevent him from being bitten again if he remembers not only the sudden movement in the park which frightens the dog and causes it to roar and bite, but also the details of the dogs soft ears and fur characteristics. The brain may well have some controlled active forgetting to prevent us from overfitting our experiences.
Are these diseases caused by overexcitement or amnesia?
Previous studies have shown that memory itself or the process of memory has gone wrong, and we believe that this kind ofunforgettableis caused by memory impairment. Common diseases in clinic are also mainly memory impairment. It is due to the necrosis of neurons in the brain. The deposition of some abnormal substances leads to memory problems. The patients can not recall the previous events, resulting in the forgetting of long-term memory. Zhu Zhizhong, deputy director of Rehabilitation Medicine Department of Tianjin Huanhu Hospital, explained that some people cant remember things because there are bugs in the process of memory. The process of memory is first cognitive knowledge, then storage, and finally extraction. Memory impairment is a problem with storage and retrieval channels. To make an image analogy, the brain is like our U disk. Memory impairment is that although we can normally copy files into the U disk, the U disk or the path of extracting files has malfunctioned, which shows that the U disk does not display any information.
However, the latest research enables us to explain these diseases related to forgetting from another perspective. Their occurrence may be caused by over excitation of forgetting mechanism or forgetting obstacles. For example, Alzheimers disease (Alzheimers disease) may be the over-activation of the forgetting mechanism, leading to the elimination of some important information. Posttraumatic stress disorder (PTSD) is caused by forgetting disorder, which can not remove bad memories in time, leading to the persistence of such psychological problems. This kind of active forgetting is like we can normally copy files into the U disk, but due to excessive cleaning or deletion, although the U disk shows no file display, but the reasons for the two same performance are quite different.
Memory and forgetting are both normal brain functions, which together maintain the balance of the brain. Zhu Zhizhong said that there are many neurotransmitters in the brain, and the regions and loops involved are particularly complex. What structures and neurotransmitters maintain the dynamic relationship between memory and forgetting? There is no experimental study to support this, and further experiments are needed to confirm it. If forgetting is really a part of the memory process that can be well controlled and innate, then if the process is out of balance, it may have a negative impact. Excessive forgetting may lead to the elimination of useful information, but also to the difficulty of trauma recovery. At present, there is no answer to the question why active forgetting occurs. (Chen Xi)