How the brain reactive emotional experiences

Key questions answered:
Q: Why are emotional memories more vivid than neutrals?
A: Because the codification of emotional memory implies a unique coordination between the amygdala and the hippocampus, which increases the force of memory.

Q: What revealed the study on brain activity during memory recovery?
A: Gamma activity patterns formed in the tonsil during emotional coding were reactivated in the hippocampus during coding and recovery.

Q: How does this discovery affect our understanding of conditions such as PTSD?
A: Identify a potential mechanism behind intrusive emotional memories, offering an objective for future treatments that could modulate or interrupt the reactivation of maladaptive memory.

Summary: A new study that uses direct recordings of human brains reveals how the tonsil and hippocampus are coordinated to form and recover emotional memories. During the aversive memory coding, the high frequency gamma activity in the tonsil shapes the response of the hippocampus, which are then reactivated in the hippocampus, but not in the tonsil, which makes the memory of memory difficult.

These patterns were linked only to emotional scenes remembered correctly and absent for neutral memories. The findings offer a mechanistic explanation of why emotionally intense experiences are often remembered more vividly and point out new therapeutic paths for memory -related disorders.

Key facts:

Tonsil units that encodes: high gamma bursts in the tonsil during the emotional experiences of the activity of the hippocampus in form. Hippocampus are reactivated: these patterns driven by the tonsil are only reactivated in the hypocament during recovery recovery.

Source: Neuroscience News

Why emotionally charged memories stay with us so vividly, while the mundane fades?

A new study that uses intracranial recordings of human patients reveals a convincing neuronal choreography between the amygdala and the hippocampus that helps to explain why aversive experiences are often recorded deeply in memory.

The research, published in Nature Communications, discovers how specific patterns of brain activity during the coding of emotional events are reactivated later during memory recovery, not in the tonsil where they originated, but in the hippocampus.

This advance not only refines our understanding of emotional memory, but can also offer information on conditions such as PTSD and anxiety.

When we experience something emotionally intense, for example, a traumatic image or a fearful encounter, our brain does not treat it as any ordinary time. Instead, it recruits specialized structures to process and store that memory in a way that ensures that it can be vividly withdrawn later.

The amygdala, associated for a long time with the processing of emotions, and the hippocampus, known for their role in memory, work together to encode these experiences. Until now, scientists were not sure how this collaboration translates into long -term memory training and subsequent recovery.

This study closes that gap, which shows how the high frequency rhythmic activity of the amygdala prints patterns that the hippocampus then uses later to reproduce the memory.

Using rare direct recordings of patients undergoing neurosurgical monitoring for epilepsy, researchers observed the brain in action as participants saw emotional and neutral scenes. Twenty -three patients had electrodes implemented in the tonsil, and fourteen of them also had coverage in the ipsilateral hippocampus.

For two days, the participants first saw scenes, some neutral, some aversive, and made basic interior/exterior judgments. A day later, they were tested in their memory for these images, categorizing them as “remembered”, “known” or “new.”

The findings were surprising. The aversive scenes remembered correctly caused a specific increase in the Gamma activity (60-85 Hz) in the hippocampus, starting approximately 0.7 seconds after the image appeared. Interestingly, the amygdala did not show this same specific gamma firm of recovery.

Instead, his role seemed to be shaped likely at the time of coding. During this phase, it was discovered that the explosions of high frequency gamma activity (90-150 Hz) in the tonsil enter hippocampus responses. These patterns were reactivated, but only in the hippocampus, during the coding of memory and subsequent recovery.

To deepen, the researchers used a method called representative similarity analysis (RSA). This approach allowed them to evaluate how brain activity patterns during recovery resembled those observed during coding.

Worldwide, Gamma activity patterns during coding and recovery were actually decorated, suggesting that at the wide level, the brain does not simply repeat the same signals.

However, when the researchers approached the phasic gamma explosions in the amygdala (transient transient activity), they found something remarkable: these precise patterns were reactivated in the hippocampus.

Even more revealing, the hippocampus not only echoed the amygdala. During the original coding, the activity of the hippocampus reflected the explosions of the phasic gamma of the amygdala with a delay of approximately 0.5 to 1 second.

Later, during recovery, the hippocampus reactivated those same specific patterns without the tonsil needing to “remember it.” In essence, the amygdala acted as a composer by establishing a musical theme that the hippocampus would perform alone alone.

The specificity of this reactivation was tested through multiple controls. For example, when the researchers observed other regions such as the lateral temporal cortex, they did not find such a reactivation pattern.

In addition, the random time windows not related to the peppers of the tonsil did not show this effect, confirming that the reactivation is specific to the structure and time.

The implications of this work are of great reach. In disorders such as PTSD, emotional memories often have fun with distressing clarity. Understanding the temporal and structural dynamics of how emotional experiences are stored and reactivated could inform new therapies aimed at weakening or modifying these memories.

Researchers suggest that cerebral stimulation strategies, such as stimulation of the theta Theta Theta, could one day be adjusted to interrupt or improve specific memory traces depending on clinical needs.

In summary, this research sheds light on a fundamental aspect of human cognition: how we remember what matters. By demonstrating that the amygdala not only indicates emotional importance, but actually prints its signature in the hippocampus, the study offers a convincing neuronal explanation of why certain moments become unforgettable. It turns out that the brain is not only a passive experience of experience, but a dynamic and highly selective narrator.

As we continue discovering how memory works at the level of brain rhythms at the scale of milliseconds, one thing is to clarify: the history of emotional memory is not just about what we feel, but when and where we feel it in the brain.

On this research news of neuroscience and emotional memory

Author: Neuroscience News Communications
Source: Neuroscience News
Contact: Neuroscience News Communications – Neuroscience News
Image: The image is accredited to Neuroscience News

Original research: open access.
“Reactivation of the human hippocampus of the gamma patterns related to the coding of the tonsil during the recovery of aversive memory” by Manuela Costa et al. Nature communications

Abstract

Reactivation of the human hippocampus of the gamma patterns related to the coding of the tonsil during the recovery of the aversive memory

Emotional memories require coordinated activity of the amygdala and the hippocampus.

Human intracranial recordings have shown that the formation of aversive memories implies a Gamma Gamma phase code of Amonla Theta-Hipocampal.

However, the mechanisms involved during the translation of aversive experiences in memories and subsequent recovery still are not clear.

Recording directly to the human tonsil and the hippocampus, here we show that the gamma activity of the hippocampus increases for correctly remembered aversive scenes.

Crucially, high amplitude gamma activity patterns in coding are reactivated in the hippocampus, but not the tonsil, both during coding and aversive recovery.

The specific hippocampus gamma patterns that show the greatest representative similarity with the activity of the tonsil in coding are reactivated in the hippocampus during the aversive recovery.

This reactivation process occurs in a context of the gamma activity that is otherwise decorcrated between coding and recovery.

Therefore, the gamma responses of the fásico hippocampus track the recovery of aversive memories, with activity patterns apparently dragged by the amygdala during coding.