Neuroscientists have recently discovered that even though the same neurons are used in the formation of different types of memory, completely different processes occur in them. This discovery could lead to the development of new and more effective treatments for negative psychological conditions like anxiety and PTSD.
The discovery challenges earlier studies that the memory of different traumatic events uses the same neurons in the same way, which in turn makes it impossible to physically distinguish between them.
To test a hypothesis explaining why memories of bad events can trigger anxiety, a team of scientists from Columbia University Medical Center (CUMC) and McGill University analyzed neurons in the molluscum Aplysia.
As you know, memory is stored in neurons. And it becomes long-term due to a kind of chemical "bridges", synapses that unite neurons into groups. Experiences about events that cause harm to the body, such as touching a hot surface or experiencing violence, are encoded into associative memory, and connections between neurons are strengthened.
However, the experience gained is not always routine. For example, while standing at the stove and hearing an unexpected doorbell, you can touch a hot stove. Or, hearing nearby dogs barking can feel like you are being attacked when you’re not. And yet, whether by accident or not you touched the slab or felt the fear of an attack, neurons record this information. And sometimes this "accidental" memory can create serious problems, acting as a trigger for anxiety, which often only aggravates the general psychological state and does not allow to cope with the real problem. Because of this random memory, many people with PTSD may relapse into traumatic emotional experiences caused by a seemingly unrelated event to the initial trauma.
“Here's an example that I love to give. Let's say you are walking through a criminal area, you decide to take a shortcut through a dark alley, and then you are robbed. Near where you ended up, you saw a mailbox. All. It will remain in your memory forever. No, not just the robbery itself. But also a mailbox. Now, when you are near the mailboxes, you can experience very strong psychological discomfort,”explains CUMC researcher Samuel Shacher.
Anxiety caused by the accidental memory of a mailbox can haunt and disrupt a person for life. A completely harmless object of urban infrastructure will trigger an uncontrolled stressful situation, while, of course, without offering a way to avoid the likelihood of being robbed in the future.
According to the "synaptic markings" hypothesis, proposed in 1997, memory is the strengthening or weakening of certain synaptic connections between neurons. Therefore, even weak stimuli are capable of leading to the formation of long-term memory, which is formed as a result of stronger subsequent stimulation of the same neuron, but through a different synaptic channel, of which, in turn, there can be several thousand. For this, special proteins must be synthesized in the nerve endings. The production of these proteins is triggered by a sufficiently strong and prolonged neuron excitation. Frey and Morris (the authors of the hypothesis) suggested that some biochemical "tags" are formed in synapses with temporarily increased conductivity. These marks, lasting no more than 2-3 hours,help to capture the desired mRNA (if the neuron begins to produce them within a specified period) and use it for protein synthesis in a given nerve ending, which ultimately leads to the transition of random memory to stable and long-term.
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Previous studies have indicated that the biochemical processes behind the formation of short-term and long-term memory, in general, have the same properties, so it is not possible to distinguish between the formation of one type of memory or another. However, if these hypothetical labels were different, this would provide a physical property that could be used later.
“One of the areas of our current research is to develop strategies to eliminate problematic non-associative memories without affecting the associative memories that can be imprinted in memory during traumatic emotional experiences. This will allow for more subconscious decision-making in the future, for example, avoiding shortcuts through dark streets in areas of high crime rates,”says Shacher.
Returning to the last study … Scientists took a pair of receptor neurons and connected them to one motor neuron (red in the image below).
One of the receptor neurons received stimulation in such a way that the process of forming a strong associative memory began. Another neuron was stimulated to induce random, non-associative memory. The researchers found that the level of strength of synoptic junction bonding was the result of the production of two different types of proteins called kinases - canase M Apl I and kinase M Apl III. Selective blocking of just one of these kinases prevented the signal from passing from the synapse to the neuron, which effectively erased a certain type of memory from existence.
Let us repeat that we are talking about neurons and synaptic connections of the mollusk aplysia. And what about the man? It turns out that vertebrates have very similar kinases involved in the formation of memory. Of course, no one says that tomorrow the pharmacy will be able to buy pharmaceuticals that will block traumatic memories, but the researchers were able to open the door, which was considered tightly closed for a long time.
“Selective memory blocking has the potential to significantly alleviate PTSD by removing non-associative memory that triggers a maladaptive physiological response,” says Jiang Yuan Hu of Columbia University Medical Center.
Perhaps, one day after the shock of a robbery, people will be able to just take a pill and forget the negative associations associated with mailboxes and barking dogs, but at the same time they will remember well, for example, the color of the attacker's jacket and other external data that will help in finding and catching criminal. Other studies suggest that the loss of random information allows our brains to store more detailed information for much longer. Even if we rule out the potential potential of new therapies, this discovery is still significant, as it allows us to better understand how our brains form long-term memory.
NIKOLAY KHIZHNYAK