Summary: Fear thoughts primarily form large organizations, but over time, they shift to be episodic memories tied to specific timelines. The dorsal prefrontal lobe after integrates the occasion sequence, which first involves the brain.
But, people with high anxiety may struggle with this connectivity, leading to continual dread and increased chance for PTSD. Understanding this process might lead to novel therapies for trauma-related problems.
Important Information:
- Over time, worry memories change from standard associations to acute sequences.
- People with high stress exhibit less strong time-based acute memory integration.
- By improving storage connectivity, this insight may aid in the treatment of PTSD.
Origin: ATR
An impressive study, to get published in , Nature Communications , on October 21, 2024, reveals the system behind two seemingly contradictory effects of fear memories: the inability to forget however the difficulty to understand.
Led by researchers from Sony Computer Science Laboratories, Inc., ATR Computational Neuroscience Laboratories, and the University of Tokyo, the research shows how dread experiences are immediately remembered as large, associated memories, but over time become integrated into sequential memories with a more specific timetable.
To monitor brain activity as participants simulated threatening events, such as a car accident, the researchers used functional magnetic resonance imaging ( fMRI ) and machine learning algorithms to conduct experiments.
They found that immediately after a fear-inducing event, the brain relies on associative memories, generalizing the fear regardless of event sequences.
However, the dorsolateral prefrontal cortex assumes a role that the hippocampus had initially led to in order to incorporate the event’s sequence into fear memory, reducing the scope of fear the day after.
The study also highlights that individuals with high anxiety, who are at greater risk for PTSD, may struggle with this memory integration. Their brains exhibit a weaker integration of time-based episodic memories through the dorsolateral prefrontal cortex, which could cause a persistent, overwhelming fear triggered by associative cues.
By focusing on the brain’s capacity to integrate episodic memories after trauma, this finding opens up new avenues for PTSD treatments.
According to lead author Dr. Aurelio Cortese of the Advanced Telecommunications Research Institute ( ATR ), “our findings reveal a previously unexplored phenomenon in how the brain prioritizes and processes fear memories.”
According to the previous author, Dr. Ai Koizumi of Sony Computer Science Laboratories, Inc.,” This time-dependent rebalancing between brain regions may explain why some people develop PTSD while others do n’t.”
The findings of the study have the potential to transform how we think about PTSD and fear-memory memories, providing fresh perspectives for developing more effective interventions.
About this research on PTSD and memory.
Author: Ritsuko Mashimo
Source: ATR
Contact: Ritsuko Mashimo – ATR
Image: The image is credited to Neuroscience News
Original Research: Open access.
Aurelio Cortese and colleagues ‘” Time-dependent neural triads between episodic and episodic cue-associative fear memories.” Nature Communications
Abstract
Time-dependent neural triads between episodic and episodic cue-associative fear memories
After traumatic events, simple cue-threat associative memories strengthen while episodic memories become incoherent. However, it is still unclear how the brain prioritizes episodic coding of traumatic events over cue associations.
In this original episodic threat conditioning paradigm, participants concurrently form two memory representations: cue associations and episodic cue sequence.
We discovered that these two distinct memories, which are competing for physiological fear expression, reorganise over the course of a long-term cue-based expression to produce precise sequence-based expression.
We use multivariate fMRI to examine how memory representations are communicated across different locations, revealing that this memory maturation is governed by a rebalancing of hippocampal- and prefrontal control of the fear regulatory circuit.
Critically, this overnight re-organisation is altered with heightened trait anxiety. We show that the brain uses selective episodic memories 24 h later but prioritizes generalisable associative memories under recent traumatic stress.
Time-dependent memory competition may , provide a unifying account for memory dysfunctions in post-traumatic stress disorders.
