How do we remember
Our brain is not a notebook in which all information is organized and can be used in any way.
Scientists have been able to identify the mechanisms of memory at the molecular and cellular level, but until nowIt is also difficult to give it a universal definition that would be suitable for the brain as a whole and for each neuron individually.
You can't even name the exact place wherememories are concentrated: in a person, almost all structures of the cerebral hemispheres are involved in recall. So the targeted and complete removal of a particular memory seems hardly possible, even in the long run.
What our memory depends on
One of the most important roles is played by the hippocampus, which can be called a temporary storage for memory, it is needed for the formation of memories and reproduction.
Damage to the hippocampus very often leads to episodic memory disordersThe example of Kent Cochrane, a famous K.C. patient who lost both hippocampi at once and lost the ability to both remember the events of his life and recall the facts of his biography.
Other types of memory, for example, semantic, which includes knowledge about facts and the structure of the world, remained practically intact with Kent.
How to block memories
Events that are associated with strong emotional experiences are remembered very well.This is due to the amygdala, which is a part of the brain adjacent to the hippocampus.
In a stressful situation, her adrenergic receptorsare activated by norepinephrine, and she herself makes the hippocampus record everything in great detail, with all the emotional nuances and associations.
Therefore, scientists have proposed to literally block traumatic memories with the help of a blocker β-adrenergic receptors, the ones that make youIn the end, the researchers opted for propranolol, widely known as a blood pressure lower.
Since the idea is to use the drug to prevent the formation of long-term, painful, emotionally charged memories of the trauma, its use is recommendedstart no later than six hours after the traumatic experience.At the same time, we must admit that in 15-20 yearsThe use of propranolol for the prevention of post-traumatic stress disorder has accumulated a significant amount of information about the effectiveness of such therapy.And the results are not so clear-cut.
How to create localized amnesia
Another interesting idea came to scientists when they investigated the mechanism of long-term memory formation.During this process, new neural connections are formed or existing ones are qualitatively changed.
These processes require protein synthesis and take a considerable amount of time—not even seconds, but minutes.
When a person receives a concussion, for examplethe brain, then it may lose some of the memories of the last minutes before the injury. This local amnesia is connected precisely with the fact that at first the memory lives only in the form of a specific pattern of neuronal activity, which disintegrates relatively easily under the influence of a sufficiently strong blow to the back of the head.
Only minutes later, the memory of the event begins to form in the structure of connections between neurons.The formation of these bonds requires the synthesis of a protein, so that its temporary blocking canIt's easy to prevent a memory from taking hold.
Work on animal models of post-traumaticDisorders show that if, after stress, the rat received an injection of a protein synthesis blocker, anisomycin, then it did not develop pronounced stress behavior subsequently.
A similar, though less pronounced, effect on the consolidation of memories isand other, safer substances:
- valproic acid,
- clonazepam,
- some cannabinoids.
Erasing destabilized memory with anesthesia
Scientists conducted a psychological experimentIn which depressed patients were shown a slideshow of an emotionally compelling story before an electric shock, researchers found that patients who went through repeated “recall” of the story before the next session remembered it significantly worse than those who did not remember it before the electric shock.
Electroconvulsive therapy is carried out under generalanesthesia, so the authors of the work suggested that the anesthetic etomidate is responsible for the decrease in memory ability. Therefore, scientists expanded the spectrum and began to study general anesthetics and their effect on memory.
This is how the authors came to the anesthetic propofol.They conducted a similar experiment as with depressed patients, and came to the conclusion that anesthesia, and not the electric shock itself, is at least partially responsible for the "erasure" of destabilized memory with electric shock.
These data are in agreement with the results previously obtained in animals.
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