Subjects: Psychology >> Developmental Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： Fear memories formed in traumatic experience is pathological basis of stress-related disorders. New memories initially persist in a fragile state and are susceptible to being disrupted by behavioral or pharmacological treatments. Exposure therapy based on extinction is a common treatment for pathological fear. However, extinction training that occurs shortly after fear conditioning is less effective than delayed extinction training in yielding long-term extinction memory, a phenomenon that is known as immediate extinction deficit (IED). The IED may be linked to levels of stress and emotional arousal at the onset of extinction training and event segmentation. If the stress and emotional arousal levels are high at the outset of extinction training, the outcomes of immediate extinction are not influenced by context change or event boundary between fear conditioning and extinction (i.e. event segmentation), but rather mainly affected by the high stress state that can impair the consolidation of extinction memory, resulting in IED. When the levels of stress and emotional arousal are moderate before the onset of extinction training, there is no difference between immediate extinction and delayed extinction, and both of them couldn’t prevent fear relapse. When the stress and emotional arousal levels are low at the time of extinction intervention, the early extinction was more effective than delayed extinction intervention, which could disrupt the consolidation of fear memory and prevent the return of fear. In addition, under moderate or low stress levels, the effect of immediate extinction would be also susceptible to event segmentation. That is, if there is a clear event boundary between fear acquisition and extinction, the event boundary may guide selective consolidation to prioritize the consolidation of emotional information in memory (fear memory) -- at the expense of related but conflicting information (extinction memory) experienced shortly thereafter, leading to IED; if without this event boundary, immediate extinction may retroactively interfere with the consolidation of fear memories and prevent the deficit; but the evidence for this is not yet sufficient. In addition, results from human fear conditioning suggest that the IED phenomenon is not inevitable, even though the electric shock was calibrated to be at the same level deemed “highly annoying but not painful” by each participant. Explanations for this may be that people's criterion for the feeling “highly annoying but not painful” has varied greatly, resulting in the actual stress and emotional arousal level of each participant is different, that is, not all participant are in a high arousal state, therefore IED phenomenon is unstable. The infralimbic (IL) that is a subdivision of the medial prefrontal cortex (mPFC) plays a key role in the consolidation and retrieval of extinction memory. The basolateral amygdala (BLA) and mPFC form strong reciprocal synaptic connections that play a key role in acquisition and extinction of fear memories. Fear extinction depends on the activities in these two projection pathways, BLA-IL and IL-BLA, which are trade-off. The neurobiological mechanisms of IED may involve that: (1) stress-induced activation of the locus coeruleus norepinephrine (LC-NE) system evokes extensive release of NE in BLA through LC-projecting neurons, leading to hyperactivity of BLA; and (2) stress-activated corticotropin releasing factor (CRF) system in BLA triggers the release of CRF that binds G-protein-coupled receptors (CRFR1), resulting in hyperexcitability of BLA; then overactive BLA inputs suppress the activity of IL via feedforward inhibition of projection neurons, which further impair the consolidation of extinction memories, causing IED. Future studies should examine whether the IED is just an aberration or early extinction acts as a secondary trauma which can continually damage the ability to extinguish fear memory, instead, contributes to the development of stress-related disorders, and explore how to optimize the clinical application of immediate extinction.
Subjects: Psychology >> Social Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： When confronted with reminders of an unpleasant memory, people often try to prevent the unwanted memory from coming to mind. Suppression-induced forgetting (SIF) means that the attempt to prevent unwanted memories from entering awareness results in a decrease in the long-term accessibility of these memories. Previous studies indicated that the suppression of retrieval is accomplished by control mechanisms that inhibit unwanted memories. Suppressing retrieval increased engagement of the right dorsolateral prefrontal cortex and middle frontal gyrus and concomitantly decreased engagement of the hippocampus. The degree of SIF is affected by the emotionality of information and an individual’s emotional state and training. From the perspective of research materials, current studies on the SIF effect of emotional memories mostly use neutral cues to match emotional materials, seldomly assess the emotional valence of cues during the learning process or after retrieval inhibition phase. More attention is paid to the memory association between cue and target event, but ignores the affective connection of them. In reality, due to the close connection between events and cues in the process of forming traumatic memories, trauma-related cues are no longer completely neutral but would have negative emotional valence. Therefore, future studies should explore the impacts of SIF on the basis of focusing on affective connection between cue and event. By individual pathological state, existing studies have investigated the SIF effect in depression and post-traumatic stress disorder (PTSD) groups, but not reached consistent conclusions. This may be related to heterogeneity of mental disorders. The people who are diagnosed with PTSD or depression will may have different etiology, symptoms and underlying neural mechanisms. Future studies should distinguish these patients into different subtypes and conduct tests in groups with the same subtypes and the same symptoms, so as to further compare the SIF effect and its neural mechanisms among different subtypes. Given that poor inhibition in patients with depression and PTSD is often associated with difficulty in activation of the right middle frontal gyrus and right dorsolateral prefrontal cortex, stimulation of the right dorsolateral prefrontal cortex may improve core symptoms in patients with PTSD. Therefore, repetitive transcranial magnetic stimulation may be used in the future to improve the activity of relevant brain regions and enhance the inhibitory control. In addition, in reality, due to the impact of stress hormones on memory consolidation, unpleasant memories are often strong and profound. Future studies may also consider the influence of stress hormones on SIF. Finally, repeated suppression training can gradually weaken the right dorsolateral prefrontal cortex-hippocampal negative coupling connections, leading to more effective control of invasive memories, suggesting the feasibility of training intervention in memory control. It has been found that mindfulness-based strategy was to facilitate the process of forgetting by releasing the tension due to the resistance to forget and aiding the reallocation of attentional resources away from the unwanted items. Therefore, future studies should consider whether the mindfulness-based forgetting strategies can improve the effect of SIF, and whether individuals who have engaged in long-term mindfulness training (such as meditation) show a better ability of retrieval suppression than those who are naïve to mindfulness practices. Future studies should investigate ways to improve the therapeutic effects of SIF on clinical pathological memory based on an in-depth understanding of the neural mechanisms of SIF.
Subjects: Psychology >> Physiological Psychology submitted time 2021-02-12
Abstract： One hallmark of posttraumatic stress disorder (PTSD) involves impairments in the ability to extinguish conditioned fear memory. Accumulating evidence suggests that extinction training that occurs shortly after fear conditioning is less effective than delayed extinction training in yielding long-term extinction memory, a phenomenon that is referred to as immediate extinction deficit (IED). However, unknown is whether the IED is just an aberration or continues to affect re-extinction. In Experiment 1, 32 Sprague-Dawley rats were randomly divided into four groups (Immediate-Extinction, Immediate-No Extinction, Delayed-Extinction, Delayed-No Extinction) and underwent a standard fear conditioning procedure in which they received five tone-footshock trials in chamber A. After either 1 h (immediate) or 24 h (delayed), half of the animals underwent 30 extinction trials (1st extinction session) in chamber B where the tone was presented alone. The other half remained in chamber B without any tone or footshock (these animals served as a no-extinction control group). Twenty-four hours later, these rats underwent the 2nd extinction session (re-extinction) in chamber B. Twenty-four hours after the 2nd extinction session, the rats were once again returned to chamber B and tested for their fear response to four continuous tones. The fear response was assessed by freezing behavior, and the effect of the 1st extinction session was assessed by the average freezing response across the first four trials of the 2nd extinction session. Compared with rats in the delayed extinction group, recently conditioned rats exhibited significantly higher levels of fear in the 2nd extinction session, although an equivalent decline in freezing was observed in both groups across the 1st extinction session, suggesting that immediate extinction failed to maintain fear suppression the next day. Furthermore, after undergoing two extinction training sessions, rats in the immediate extinction group exhibited no significant reduction of freezing compared with the non-extinguished control during the retention test, suggesting that the deficit reappeared during re-extinction. The aim of Experiment 2 was to investigate whether the deficit that was induced by immediate extinction could be rescued by the β-adrenergic receptor antagonist propranolol. In Experiment 2, 20 Sprague-Dawley rats underwent the same procedures as the immediate extinction groups in Experiment 1, with the exception that they received saline or propranolol (10 mg/kg, i.p.) within minutes after fear conditioning. We found that one injection of propranolol immediately after fear acquisition rescued the deficit of re-extinction but not immediate extinction. This study revealed that the early extinction intervention after severe trauma may not only fail to inhibit the fear response but also act as a secondary trauma which can continually damage the ability to extinguish fear memory. Propranolol may be a good candidate to repair such damage. Our findings improve our understanding of the pathogenesis of PTSD and outcomes of an early intervention and may be helpful for selecting appropriate and effective interventions after trauma exposure and avoid secondary trauma that is caused by the intervention itself. "
Subjects: Psychology >> Physiological Psychology submitted time 2020-11-30
Abstract： When confronted with reminders of an unpleasant memory, people often try to prevent the unwanted memory from coming to mind. Suppression-induced forgetting (SIF) means that the attempt to prevent unwanted memories from entering awareness results in a decrease in the long-term accessibility of these memories. Previous studies indicated that the suppression of retrieval is accomplished by control mechanisms that inhibit unwanted memories. Suppressing retrieval increased engagement of the right dorsolateral prefrontal cortex and middle frontal gyrus and concomitantly decreased engagement of the hippocampus. The degree of SIF is affected by the emotionality of information and an individual’s emotional state and training. Future studies should investigate ways to improve the therapeutic effects of SIF on clinical pathological memory based on an in-depth understanding of the neural mechanisms of SIF. "
Subjects: Psychology >> Physiological Psychology submitted time 2020-08-18
Abstract： Extinction training that occurs shortly after fear conditioning fails to yield long-term extinction memory, a phenomenon that is known as the immediate extinction deficit (IED). The IED may be linked to levels of stress at the onset of extinction training and event segmentation. Under high levels of stress, the consolidation of extinction memory is impaired, resulting in the IED. Under moderate or low levels of stress, immediate extinction would be effective but susceptible to event segmentation. The neurobiological mechanisms of IED may involve stress-induced activation of the locus coeruleus norepinephrine system, which leads to hyperexcitability of the basolateral amygdala and the subsequent inhibition of activity of the medial prefrontal cortex (i.e., a region that plays a central role in fear extinction) through synaptic projections. Future studies should consider long-term outcomes of the IED and optimization of the clinical application of immediate extinction.
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