Remembering the good, while forgetting the bad
The effect of a stressor and sex-differences in the intentional control of memory.
Hugo Langeveld (10770232)
Daily supervisor: Conny Quaedflieg, PhD
Abstract
This study is the first to investigate the effect of acute stress on the intentional control of memory. Deficits like Post Traumatic Stress Disorder (PTSD) and depression are found with impaired suppression of negative thoughts. Suppression of negative thoughts and repetition of positive thoughts lead, respectively, to forgetting and enhancement of your memory. Associated with intentional memory control is the dorsolateral prefrontal cortex (dlPFC) which its function impairs under stress. To test intentional memory control the “think/no-think” paradigm was used. A differential effect of stress on the intentional control of memory was found, with an enhancing effect of stress on memory performance. This is not in line with the stress
impairments with stress-related diseases and on the moleculaire level. Although, unless inconsistent results, memory reconsolidation enhances memory performance after stress. Future studies should determine salivary measurements to critical reflect on the stress inductio and the effect of stress on memory retrieval.
1. Introduction
To a certain extent, we do have power over our memory recollections: intentional memory control. Active intentional memory control comprises the repeated intentional retrieval (‘positive control’) or suppression (‘negative control’) of memories, leading to memory enhancement or intentional forgetting (Anderson & Green, 2001). Intentional memory control is adaptive, helping us to remember things we wish to remember, while suppressing memories that pose a threat to our well-being (Anderson & Hanslmayr, 2014).
The ability to intentionally control memory varies with individual differences and defects in this ability are seen in stress-related disorders. For instance, a deficit in negative memory control has been shown in depression and Post Traumatic Stress Disorder (PTSD) (Catarino et al., 2015; Hertel & Gerstle, 2003). Stress has impact on several cognitive functions, like attention and social cognition (Diamond et al., 2007), but particular learning and memory are well documented in the literature to be affected by stress (Roozendaal et al., 2009). This study investigated the effect of acute stress on our ability to control our memories.
1.1 ANS and HPA axis activation
In reaction to acute stress two systems are activated the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal (HPA) axis. Jointly, these systems enable the individual to adjust the response to the stressor (De Kloet et al., 2005). Catecholamines in the sympathetic nervous system are released by the ANS, thereby stimulating arousal, alertness, and focused attention that normalizes soon after stressor offset (i.e., it lasts only several minutes) (Ulrich-Lai & Herman, 2009). The second major stress system, the hypothalamic-pituitary-adrenal (HPA) axis, responds slower and the levels of its end product cortisol remain increased for a longer time (i.e., minutes to hours). The end product of these two stressor systems, cortisol, is produced by the adrenal glands, transported via the blood flow, and affects corticoid receptors in the brain.
1.2 The cellular stress response
Cellular responses to acute stress are mediated through the intracellular Glucocorticoid Receptor (GR) and Mineralocorticoid Receptor (MR) in the hypothalamus, hippocampus, prefrontal cortex and amygdala (Groeneweg et al., 2011). The MR has an 10-fold higher affinity for corticosterone (cortisol in humans) than the GR what results in a dense MR occupancy rate in basal, not stressful,
concentrations of corticosterone. Corticosterone negatively feeds back on the HPA-axis in a genomic response (De Kloet et al., 1998) mediated through slow genomic transcriptional regulation (Joëls & Baram, 2009). On the other hand, HPA-axis activity is regulated through non-genomic rapid responses mediated by post-synaptic stimulation of glutamate (Groeneweg et al., 2011) minutes after the stressor.
Spontaneous release of glutamatergic vesicles from the pre-synaptic site on the post-synaptic site are reflected by miniature excitatory postpost-synaptic sites (mEPSPs) (Bekkers & Stevens, 1989). EPSPs are known to play a major role in post-synaptic activation, and thereby stimulating the limbic areas in the brain for long-term potentiation (LTP) (Yuen et al., 2009). LTP in synapses is elicited by the activation of the post-synaptic NMDA-receptors, which stimulate the synthesis of new proteins that triggers changes in synaptic function (Lüscher & Malenka, 2012) what is associated with learning and memory processes in the brain (Mayford et al., 2012). Tasker & Malcher-Lopes (2006) found that a high dose of corticosterone (between 100 nM and 1 uM) reduces the post-synaptic mEPSPs in hypothalamic neurons.
Salivary cortisol responses due to psychological stress in females were modulated by the menstrual cycle, where salivary responses in the luteal phase were equal to men, but not in the follicular phase (Kirschbaum et al., 1999). The variation in the psychological stress response by sex is probably related to differences in internal endocrine milieu. An hormone that is known to affect the cortisol response to psychological stress is ethinyl estradiol (EE2), and is found in oral contraceptives (Kumsta et al., 2007). EE2 stimulates the production of corticosteroid binding globulin (CBG) what reduces free cortisol levels in the blood.
1.3 Impact of stress on memory
Declarative memory formation is hippocampal-dependent and enhanced under stress through the MR (Karst et al., 2005). After, memories are connected and wired around the neocortical areas for long-term memory formation where memories can be experienced and recalled. There are three declarative memory phases: encoding, consolidation and retrieval. On the one hand, stress enhances memory encoding and consolidation, if the stress is congruent of time and context, due to GR activation in the basolateral amygdala (Schwabe et al., 2010). On the other hand, memory retrieval is impaired by elevated cortisol levels while retrieving emotionally arousing pictures (Buchanan & Tranel, 2008).
Estrogens are found to neutralize the glucocorticoid effects after stress (Mizoguchi, 1992). Confirmed in the study of Carlson & Sherwin (1999) where elderly females without hormone replacement therapy showed worse declarative memory retrieval compared to elderly females with hormone replacement therapy. After the menopauze the internal endocrine milieu of female changes, where 30-50% of female above 85 suffer from dementing processes (Bachman et al., 1992).
1.4 The control of memory
Anderson & Green (2001) developed the “think/no-think” (T/NT) paradigm that tests intentional control of memory. In this paradigm effective inhibitory control through the ability to withhold a response is measured with the “go/no-go” paradigm to test executive control over motor actions in a memory retrieval task. Hereby, suppressed cues have a larger effective inhibitory control compared to repeated cues, and are less remembered - better forgotten, and vice versa.
A functional Magnetic Resonance Imaging (fMRI) study of Anderson et al. (2004) found a decreased activation of the hippocampus by recalling forgotten items. During suppression trials an activated right dorsolateral prefrontal cortex (dlPFC) was found. The dorsolateral prefrontal cortex plays a role in high-order cognitive performance, like working memory (Goldman-Rakic, 1987) and executive control (Garavan et al., 1999). Inducing forgetting of suppressed content is found by the downregulation of hippocampal activity of the dlPFC (Anderson & Hanslmayr, 2014). Schmitz et al. (2017) found in a H magnetic resonance spectroscopy greater resting concentrations of hippocampal GABA correlating with better mnemonic control.
Diseases like PTSD also show impaired functioning of the intentional memory control (Aupperle et al., 2012). Though the effect of stress on intentional memory control has never been investigated. The aim of the current study is to investigate the effects of stress on the intentional control of memory and whether there are difference between men and women. Because of the impaired function of the dlPFC under stress and the impaired function by stress-related diseases like PTSD, we hypothesize that acute stress impairs intentional memory control. In other words, no difference between the items in the T/NT-paradigm are expected in the stress condition. Secondly, we hypothesize that gender affects intentionally memory control after stress, where women have smaller intentional memory control effects than men by binding free cortisol due to oscillatory levels of estradiol in the menstrual cycle.
2. Methods 2.1 Participants
28 healthy male and female graduates (mean age = 22.33 years, SD = 3.22; range: 18-35 years) were acquired via advertisements at the Maastricht University. Participants were excluded if they had a history of psychiatric, cardiovascular, autoimmune, neuroendocrine or metabolic diseases, were considered smokers (i.e., more than ten cigarettes a week), were considered drinkers (i.e., more than ten 0.25 cL 5% alcohol drinks a week), used drugs more than once per month, used medication known to affect the ANS or HPA axis, were vaccinated within a period of two months before testing, or had a body mass index (weight in kg/(height in m)^2) outside the 18-28.5 range. Test protocols were approved by the standing ethics committee of the Faculty of Psychology and Neuroscience, Maastricht University. Participants were rewarded for their participation with course credits or little monetary contribution.
2.2 Stress manipulation
The Maastricht Acute Stress Test (MAST) has been designed to combine both physical and psychological stressors (Smeets et al., 2012). The MAST is a combination of exposure to ice cold water and a mental arithmetic task. In the stress condition, the water temperature is four degrees Celsius (using an electrical cooler and a circulation pump (JULABO Labortechnik, Seelbach, Germany) in a plexiglas box. In the mental arithmetic task, participants had to deduct as fast and accurate as possible in steps of seventeen from randomly chosen numbers and corrected with social-evaluative pressure (i.e., negative feedback). Participants were told that there facial expression will be videotaped during the experiment for later analyses. In the no-stress control condition the water temperature is around 36 degrees of Celsius and the participants had to count, in their own speed, from one till 25, and start again at one when reaching 25 without social-evaluative pressures nor being videotaped. To increase unpredictability and uncontrollability alternating hand immersion and arithmetic trials are told to be randomly chosen by the computer and the duration is minimum 45 and maximum 90 seconds.
2.3 Subjective stress response
Prior and after the MAST negative mood was assed using the Positive and Negative Affect Schedule, state version (PANAS; Watson et al., 1988). The PANAS consists of two subscales that quantify current positive affect and negative affect scale from one (very slightly) to five (extremely). The scores on the positive and negative subscale
are related to each other, where a high score on the Negative Affect subscale a lower score on the Positive Affect scale indicates and vice versa. Additionally, subjective ratings after the MAST were assessed using VAS scores implying scales of pain, stress and unpleasantness.
2.4 Physiological ANS response
The physiological ANS response was measured using blood pressure and changes of heart rate over time. Diastole blood pressure (DSB), systole blood pressure (SBP) and heart rate were measured five times, before and after the stress induction (tbaseline vs. tpre-stress vs. tstress vs. t+25 vs. t+40). During the stress induction (tstress) the physiological ANS response were measured before, at the second hand immersion trial and at the end. The palpatory estimation of the blood flow was done seated with (Omron M7) on the same arm.
2.5 Physiological HPA response
The unbound cortisol in saliva was measured in response to the stress induction by synthetic Salivette (Sarstedt, Etten-Leur, The Netherlands) devices twice before and 10, 25 and 40 minutes after the MAST or no-stress condition task. Samples were stored in a fridge at minus 20 degrees Celsius before they were analyzed. A cortisol increase, compared between the five measurements, equal to or larger than 2.5 nmol/ l (see, for example, Kirschbaum et al., 1993; Smeets et al., 2012), is thought to reflect a cortisol secretory episode (van Cauter & Refetoff, 1985) and was set for the threshold of a physiological HPA response induced by stress.
Cortisol concentrations were determined by the IBL International Luminescence Immunoassay protocol (IBL, Hamburg, Germany). Luminescence immunoassay is based on the competition principle where an unknown amount of antigen present in the sample (20 µL) and a fixed amount of enzyme labelled antigen (100 µL) compete for the binding sites of the antibodies coated onto the wells. The reaction in the wells was covered with adhesive foil and incubated for 3 hours at room temperature (18-25°C). The competition reaction was stopped by washing the plates four times with 250 µL of diluted Wash Buffer. The residual solution was removed by tapping the inverted plate on a paper towel. Fifty µL of Substrate Solution Mixture was added where after ten minutes the relative Luminescence, inversely proportional to the amount of the antigen in the sample, was determined with a Luminometer. Results of
samples were determined directly using the standard curve. A minimum of 0.5 mL liquid from the Salivette should be collected.
2.6 Intentional Memory control Task
Participants were presented with eighteen corresponding cue and targets consisting of small fragments of episodes from the serie ‘The Big Bang Theory’. These cue-target pairs were learned in phase 1, the encoding phase, were manipulated in phase 2, the think/no-think phase and were retrieved in phase 3, the recall phase.
In encoding phase 1 the cues and targets were shown twice in sequential order. After the participants were scored on elements in the target scene in an intermediate time of forty seconds, between the cue and the target. In response the target was shown directly after to serve as feedback.
In think/no-think phase 2 two-third of the cue-target pairs were instructed with “Think” or “No-think”. Both instructions were showed, in green (“Think”) or red (“Do NOT-Think”), before the cue appeared. “Think” instructed silent visualization of the corresponding target, if participants had troubles visualizing they were instructed to search in their memory. “No-Think” instructed silent suppression of the corresponding target. Participants were told not to distract their thoughts nor close their eyes. The cue was shown ten seconds to either visualize or suppress the target. A practice with three cue-target combinations was included to let participants fully understand the task. Each associated fragment was suppressed or visualized eight times in a randomized order to avoid mood induction.
In the recall phase 3 fifteen cues, the practice cues were left out, were presented in sequential order. The effect of the “Think” and “No-Think” items were measured in relation to cue-target combinations without instruction - baseline items. Performance of phase 1 and 3 was scored in 84 points reflecting the scene as well the dialogues of the target fragment. Both scenes and dialogues were given a point, where the maximum given points between the trials differed.
2.7 Procedure
In figure 1 an overview of the procedure is shown. Participants were semi-randomly divided in two conditions, stress or control as participants were excluded to the stress condition and assigned to the control condition if they had participated in other studies with water lately or participated in other parallel study of taste perception at
Maastricht University. Cortisol fluctuations due to circadian rhythm was controlled by testing between 12:30 and 6 pm. Besides participants were asked to hold off from drinking anything except non-sparkling water, eating and heavily exercising two hours before the experiment what prevented fluctuations in the cortisol level. These criteria were tested when participants arrived in the laboratory by filling in a form on both days.
After their arrival in the laboratory participants gave written consent to participate in this study. First a mood state questionnaire was filled out. After the Stroop task and the Digit Span task were performed as indicator of working memory performance. After these tests a baseline cortisol and blood pressure measurements were taken. The encoding phase 1 of the T/NT paradigm demanded a minimum amount of points (i.e., 59 points, 70%) after three learning sessions. When participants did not meet this requirement they were excluded from the experiment and received little monetary fee or course credits.
The participants returned twenty-four hours after the T/NT phase 1 to the lab. The eighteen cues and targets were shown once, where after pre-stress saliva and blood pressure measurements were taken. Prior and after the MAST or the no-stress control condition the PANAS was filled out. Ten minutes after the MAST, a saliva sample was taken. The T/NT task phase 2 consisted of two blocks with a saliva sample and blood pressure measurements in between. Finally, participants performed the retrieval test, in recall phase 3. After, participants filled out questionnaires. At the end they were debriefed and thanked for their participation.
2.8 Statistical analysis
The effect of condition (stress vs. control) x timing (PANASpre vs. PANASpost) analysis of variance (ANOVA) were analyzed for subjective stress ratings with timing as within factor. Blood pressure stress responses were analyzed using the between factor condition (stress vs. control) and the within factor time (tprestress vs. tstress vs. tpoststress) analysis of variance (ANOVA).
For the effect of sex on the percentage learned items a mixed design model made up of two between-subject factors condition (stress vs. control) and sex (male vs. female) and within-subject factor (instruction: “Think”, “No-think” and “Baseline”). For the effect of condition on the percentage learned items and intentional memory control a mixed design model made up of between-subject factor condition (stress vs. control) and within-subject factor (instruction: “Think”, “No-think” and “Baseline”). Pearsons’s correlations between participants’ physiological stress response and positive or negative memory control were conducted. An outlier with a correlation coefficient with a value four and a half times bigger than the largest correlation coefficient was removed. Cohen’s Partial Eta Squared was calculated as a measure of effect size. Post-hoc tests were performed with a Bonferroni correction for multiple comparisons in case of significant interactions.
3. Results
3.1 Stress Manipulation
For subjective stress, the PANAS Negative Affect a non-significant interaction between gender, condition and time was found (F(1,40) = .07, p = .80), and a significant interaction between condition and time was found (F(1,48) = 8.81, p = .005; η2p= . 67) and a non-significant main effect of sex (F(1,50) = .21, p = .65). Simple effect analysis per time point revealed that for baseline the main effect of condition was not significant (F(1,24) = .14, p = .91) while groups did differ after the MAST (F(1,24) = 11.81, p = .002; η2p= 1.40) with higher negative affect values in the stress group. The PANAS scores in time point per condition are shown in figure 2.
In figure 3 the VAS scores following the MAST or no-stress condition are shown. For subjective stress, a non-significant interaction between gender and time (F(1,74) = 2.96, p = .09), a non-significant main effect of gender (F(1,76) = .99, p = .32) and a significant main effect of condition (F(1,76) = 99.66, p < .001; η2p= 2.29) was found.
For physiological stress, gender, condition and timing did not differentially affect the blood flow measurements, as indicated by the non-significant gender x condition x time: (-pre, during and after) interaction (heart rate: F(1,66) = .07, p = .93, DSB F(1,66) = 1.49, p = .23, SBP F(1,66) = .45, p = .64). Condition and timing did not differentially affect the blood flow measurements, as indicated by the non-significant condition x time interaction (heart rate: F(1,75) = .37, p = .69), DSB (F(1,75) = .53, p = .59) and SBP (F(1,75) = .72, p = .49). A significant main effect of the condition in DSB F(1,82) = 20.11, p <.001; n2p = .99 was found, where values under stress were higher. Heart rate and DSB measurements per time point in stress and control condition are shown in figure 4 and SBP measurements are shown in figure 5.
3.2 T-NT learning phase
Sex, condition and item type did not differentially affect the learned scores, as indicated by the non-significant sex x condition x item type interaction (F(1,72) = 2.48, p = .09). For the learning phase the split-plot ANOVA with item (think vs. no-think vs. baseline) and condition (stress vs. control) revealed that condition did not differentially affect the percentage learned items, as indicated by a non-significant interaction effect (F(1,81) = .55, p = .58), a non-significant main effect of item type (F(1,87) = .15, p = .87) and a non-significant main effect of condition (F(1,88) = 3.10, p = .08). For sex a non-significant main effect (F(1,88) = .01, p = .98) was found. Percentage learned items per condition are shown in table 1 below.
Intentional memory control under stress
For the recall phase the split-plot ANOVA with item (think, no-think and baseline) and condition (stress and control) revealed that condition did not differentially affect the percentage recalled items, as indicated by a non-significant interaction effect (F(1,81) = .53, p = .59), a non-significant main effect of item type (F(1,87) = .40, p = .68) and a significant main effect of condition (F(1,88) = 17.19, p < .001; n2p = .88), with higher mean scores in the stress (86.43) than the control group (75.21). As we used a adapted TNT paradigm, exploratory analysis in the control condition were performed. The repeated measures ANOVA revealed a non-significant main effect of item type (F(1,43) = .31, p = .53). Percentage recalled items per condition are shown in figure 6 and 7 below.
3.3 Intentional memory control and sex
Sex, condition and item type did not differentially affect the recall scores, as indicated by the non-significant sex x condition x item type interaction (F(1,48) = .38, p = .54) and a non-significant main effect of sex (F(1,58) = .02, p = .90). Means per item between condition and gender are shown in table 2.
3.4 Associations between stress and intentional memory control
Pearson’s correlation between stress measures (DSB, SBP and heart rate) and the difference scores of the items in positive control (Think minus Baseline), negative control (No-Think minus Baseline) and total control (Think minus No-Think), in the stress or control condition, were determined. A significant positive correlation (r = . 66, p = .02) between SBP and positive control in the control condition was found, indicating higher SBP in non-stress condition results in larger positive control effect. The correlation between positive control and SBP was not significant in the stress condition (r = .08, p = .77). None of the other correlations scores were significant. These results are shown in figure 7 and 8 below.
4. Discussion
The primary aim of the current study was to investigate the influence of stress applied on long-term (24 hour) intentional memory control. Results demonstrate that participants in the stress condition displayed significant stress responses in terms of subjective negative affect and VAS scores compared to the no-stress control condition. This is in line with Smeets et al. (2012). However, Smeets et al. (2012) found a significant effect of condition on DBP, SBP and heart rate measurements, where we only found an effect of DBP measurements before and after the MAST. A non-significant reason could be the low experimental size (n=30) compared to (n=80) from Smeets et al. (2012). Additionally, misclassification of cortisol responders and not responders could also explain differences in the findings. In our experiment no salivary measurements were done, so the classification of cortisol responders and not responders only relied on the PANAS scores, VAS scores and blood pressure measurements. Smeets et al. (2012) classified responder with a cortisol increase equal to or larger than 2.5 nmol/l. Domes et al. (2002) found a improved declarative memory by high cortisol responders (6.18±11.24 nmol/l) compared to low cortisol responders (0.21±3.90 nmol/l).
Learning scores were not affected by sex, condition and item type. In general around 72%, after three learning trials, of the total items (n=84) were learned. Compared to Anderson & Green (2001) word pair study, only half of the items were learned. A higher percentage learned items could better detect effects of intentional memory control and condition on recall scores.
The exploratory analysis in the control group revealed no significant effect of item type on intentional memory control, indicating no effect of the positive, negative and total control on memory retrieval. This is not in line with Anderson & Green (2001) who found impaired memory-induced forgetting and improved memory retrieval by, respectively, suppressing and responding the cue. Only, Anderson & Green (2001) tested on the same day, whereby the positive and negative control effect could be due to memory consolidation or retrieval. Despite, a non-significant reason could be the use of videos instead of word pairs. Although videos were chosen, because of the visual representation of stimuli what enhances memory retrieval (Kelley et al., 1998). Corresponding with our results Lui et al. (2016) found less induced forgetting of intentional forgetting after long-term (24 hours) memory formation due to less
hippocampal-dependent memory activation. Individual differences in intentional control of memory were not taken into account, where determination of resting hippocampal GABA concentrations could fulfill that. Future studies should take the resting hippocampal GABA concentrations into account, to take along individual differences of intentional control of memory, combined with visual representations in the T/NT-paradigm without long-term (24 hour) memory formation on memory retrieval with the classification of cortisol responders and not responders.
A differential effect of condition on intentional memory control was found, where recall scores in the stress group (86.43) were higher than in the control group (75.21). Our results are not in line with Catarino et al. (2015) who found an impairing effect on memory retrieval by PTSD patients and Hertle & Gerstle (2003) who found an impaired effect of memory retrieval by depression as well. These studies are in line with expected non-genomic effects of a stressor. Either stress in this experiment affected the T/NT phase 2, and thereby the manipulation of the consolidated memories instead of the memory retrieval and could cause the enhancing memory retrieval under stress. An explanation could be memory reconsolidation, either the results are inconsistent in the field. One study showed that acute stress after reactivation of autobiographical memories impaired the memory for the neutral episodes 1 week later (Schwabe & Wolf, 2010). However, another study stated that stress after reactivation enhanced memory performance for neutral and emotional words (Bos et al., 2014).
In general sex did not affect the intentional control of memory, the learning scores and the stress manipulation. This is not in line with Kirschbaum et al. (1999) who found different stress responses and Carlson & Sherwin (1999) for memory retrieval in female due to the oscillatory estradiol levels of the menstrual cycle. A non-significant reason could be the take of hormonal birth contraceptives, what could have stabilized the estradiol levels and resulted in tolerant cortisol effects by women.
A significant positive correlation between SBP and positive control in the control condition was found. Indicating that higher SBP values correlated with a larger positive control effect. In the stress group a slightly negative trend line between SBP and positive control, but no correlation was found. This is in line with our hypothesis that stress impairs the function of the dlPFC what impairs intentional control of
memory.
A limitation of the current study is worth mentioning. Participants were tested on two consecutive days, were on the second day the testing took more than 90 minutes. On this second day they also had to concentrate twice for thirteen consecutive minutes on the “think/no-think”-task, seeing the cues eight times. These long periods of concentration and frequent stimuli could have caused mood induction, thereby influencing the memory consolidation and eventually memory retrieval. This was often notified in the notes of the experimenter during testing. Mood state induction could be reduced by implementing more cues and targets in the learning phase or smaller blocks of the T/NT phase 2.
In sum, the results of this study suggest that stress enhances memory retrieval performance after intentional control of memory. This was not in line with the rapid non-genomic effects after stress, the impairing dlPFC functioning under stress and the impaired intentional control of memory by PTSD patients, but, unless the inconsistent findings in the field, memory reconsolidation enhances memory performance after stress. Gender does not affect the intentional memory control, learning scores and stress manipulation. Estradiol neutralizes glucocorticoid effects after stress, which are oscillating in the menstrual period by females, indicating different levels of tolerance. Hormonal contraceptives could have stabilized this neutralizing effect of estradiol. This is the first study investigating the effect of stress on intentional memory control and more studies are needed including studies looking into the mechanisms of individual differences determined by hippocampal GABA concentrations, biological markers for the stress induction of cortisol responders, the long-term (24 hour) consolidation of intentional memory control and visual representation of the stimuli for a better understanding of intentional memory control.
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