Subjects: Psychology >> Medical Psychology submitted time 2023-11-02
Abstract： Memory is stored in the strength changes of synaptic connections between neurons, and neurotransmitters play a crucial role in regulating synaptic plasticity. Neurons expressing specific types of neurotransmitters can form distinct neurotransmitter systems, including the dopaminergic, noradrenergic, serotonergic, and glutamatergic systems. Studies on the destabilization processes of various types of memories have revealed the important role of acetylcholine in memory destabilization triggered by the retrieval of novel associative information. The resistance of high-intensity fear memories to destabilization and reconsolidation is attributed to the activation of the noradrenergic-locus coeruleus system during the encoding process of such fear memories. Other important neurotransmitters, such as dopamine, glutamate, gamma-aminobutyric acid (GABA), and serotonin, also exert influences on memory plasticity at different stages of memory formation. Neurotransmitters play significant roles in fear memory destabilization and reconsolidation, but these effects are typically not independent; rather, they involve interactions and mutual regulation, such as dopamine-cholinergic interactions and serotonin-glutamate interactions. Furthermore, this summary elaborates on the roles of the aforementioned neurotransmitters in memory reconsolidation and their interactions. The study of neurotransmitters at the molecular level can provide valuable insights for the investigation of interventions targeting fear memory reconsolidation. In the future, research should continue to explore the key factors and methods underlying fear memory destabilization based on the molecular mechanisms of memory destabilization and the role of neurotransmitters, to improve the clinical treatment of PTSD based on the reconsolidation intervene.
Peer Review Status:
Awaiting Review
Subjects: Psychology >> Medical Psychology submitted time 2023-11-01
Abstract： According to the error-driven learning theory, the mismatch between expected outcome of behavior and actual result, known as “Prediction error” or PE, is the driving factor of new learning. Prediction error differs from other types of salience, such as physical salience, surprise, or novelty, in terms of distinct periods of information processing, as well as in its relationship with memory updating. The reconsolidation interference paradigm has been shown to be effective in neutralizing conditioned fear memory in humans, where the prediction error involved in memory reactivation is required to reactivate memory for reconsolidation. In the behavioral mechanisms of PE in promoting fear memory updating, it is found that PE is a necessary but not sufficient condition of memory destabilization. Memory reactivation must include appropriate degree of PE; however, properties of the memory must be taken into account when determining the fate of memory following reactivation, which could be destabilization, extinction or limbo. In the neural mechanism of PE in fear memory updating, amygdala, periaqueductal gray (PAG) and hippocampus are found to play an important part in PE detection and computation. The prefrontal cortex (PFC) and its subregions play a crucial role in the process of PE-initiated memory reconsolidation. Furthermore, some essential neurotransmitters in the nervous system are involved in this process, notably dopamine and glutamate. In the future, quantitative investigations based on statistical calculation models of PE need to be conducted to explore the interactions between PE and other boundary conditions on memory reconsolidation. The role of different types of salience in memory reconsolidation is also worth investigating. In addition, individual difference in PE’s role in updating fear memories must be taken into account to facilitate clinical translations. In both basic research and therapeutic intervention attempts, we feel that multidisciplinary techniques and procedures are essential for elucidating the processes underlying the involvement of PE in fear memory reconsolidation and updating.
Subjects: Psychology >> Medical Psychology submitted time 2021-02-05
Abstract： Under the framework of Reconsolidation Interference of conditioned fear memory, Prediction Error (PE) is demonstrated as a necessary condition of memory destabilization. However, the role of PE in destabilizing fear memories of different strength is unclear. The degree of PE that is needed to effectively reactivate fear memory may be changeable according to the strength of memory. It is unknown whether the PE used to reactivate weak memories is still valid in retrieving enhanced memories. Besides, explorations of possible solutions are rare if strong memories are resistant to undergoing reconsolidation. Among factors that are possible to help to overcome the boundary condition, the effects of stress hormone are worth exploring. However, the manipulation of fear strength in human studies in the laboratory has not been well developed. Thus, the present study has three main aims: (1) based on previous results in animal studies, we tested the effect of fear memory strength manipulation in the laboratory settings in humans; (2) to examine the effect of PE during reactivation on destabilizing different strength memories and (3) to test the possible influence of post-reactivation exogenous stress to the retrieval-extinction of fear memories. The three days retrieval-extinction paradigm was adopted in the present study. We manipulated the memory strength through two kinds of acquisition procedures on the first day, which varied the predictability of the unconditioned stimulus (US) occurrence after the conditioned stimulus (CS). 24 hours later, a reminder contained a single PE was used to reactivate memories, then followed by a stress task (Social Evaluate Cold Pressor test, SECPT) or not before extinction. After 24 hours, a test of spontaneous recovery and reinstatement was utilized to measure the return of fear in each condition. All participants were divided into three conditions: CS-Predictable US_no Stress Group, CS-Unpredictable US_no Stress Group and the CS-Unpredictable US_Stress Group. The skin conductance response (SCR) and fear-potentiated startle response (FPS) were used as measurements of conditioned fear. The results showed that there was a relatively higher increase in fear response (SCR) from Day 1 to Day 2 in the CS-Unpredictable US condition than the CS-Predictable US condition, which may suggest the difference of memory strength among conditions. And for the weak fear memory (CS-predictable US), the reactivation that contained single PE and followed by extinction training can prevent the spontaneous recovery, especially on the SCR measurement. While in the enhanced memory condition (CS-unpredictable US), the extinguished memory had a distinct relapse in the memory test on the third day, which suggests the failure of memory destabilization. Furthermore, under this condition, if the acute stress task was adopted after reactivation, the return of fear would further increase, comparing with the no stress manipulation conditions. These results indicate that PE used to reactivate weak memories is insufficient to destabilize strong memories; and the post-reactivate acute stress cannot compensate this deficit caused by boundary conditions (e.g., strength). We further discussed possible interpretations of these results and the implications for the translation of retrieval-extinction to clinical practice and the cure of post-traumatic stress disorders (PTSD).
Peer Review Status:Awaiting Review
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