Stress is a constant characteristic of everyday life in our society, playing a role in triggering several chronic disorders. Therefore, there is an ongoing need to develop new methods in order to manage stress reactions. The regulatory function of right medial-prefrontal cortex (mPFC) is frequently reported by imaging studies during psychosocial stress situations. Here, we examined the effects of inhibitory and excitatory preconditioning stimulation via cathodal and anodal transcranial direct current stimulation (tDCS) on psychosocial stress related behavioral indicators and physiological factors, including the cortisol level in the saliva and changes in brain perfusion. Twenty minutes real or sham tDCS was applied over the right mPFC of healthy subjects before the performance of the Trier Social Stress Test (TSST). Regional cerebral blood flow (rCBF) was measured during stimulation and after TSST, using pseudo-continuous arterial spin labeling (pCASL). Comparing the effect of the different stimulation conditions, during anodal stimulation we found higher rCBF in the right mPFC, compared to the sham and in the right amygdala, superior PFC compared to the cathodal condition. Salivary cortisol levels showed a decrease in the anodal and increase in cathodal groups after completion of the TSST. The behavioral stress indicators indicated the increase of stress level, however, did not show any significant differences among groups. In this study we provide the first insights into the neuronal mechanisms mediating psychosocial stress responses by prefrontal tDCS.

OBJECTIVE: Aromas may improve physiologic and cognitive function after stress, but associated mechanisms remain unknown. This study evaluated the effects of lavender aroma, which is commonly used for stress reduction, on physiologic and cognitive functions. The contribution of pharmacologic, hedonic, and expectancy-related mechanisms of the aromatherapy effects was evaluated. METHODS: Ninety-two healthy adults (mean age, 58.0 years; 79.3% women) were randomly assigned to three aroma groups (lavender, perceptible placebo [coconut], and nonperceptible placebo [water] and to two prime subgroups (primed, with a suggestion of inhaling a powerful stress-reducing aroma, or no prime). Participants' performance on a battery of cognitive tests, physiologic responses, and subjective stress were evaluated at baseline and after exposure to a stress battery during which aromatherapy was present. Participants also rated the intensity and pleasantness of their assigned aroma. RESULTS: Pharmacologic effects of lavender but not placebo aromas significantly benefited post-stress performance on the working memory task (F(2, 86) = 5.41; p = 0.006). Increased expectancy due to positive prime, regardless of aroma type, facilitated post-stress performance on the processing speed task (F(1, 87) = 8.31; p = 0.005). Aroma hedonics (pleasantness and intensity) played a role in the beneficial lavender effect on working memory and physiologic function. CONCLUSIONS: The observable aroma effects were produced by a combination of mechanisms involving aroma-specific pharmacologic properties, aroma hedonic properties, and participant expectations. In the future, each of these mechanisms could be manipulated to produce optimal functioning.

Corticosteroids, released in high amounts after stress, exert their effects via two different receptors in the brain: glucocorticoid receptors (GRs) and mineralocorticoid receptors (MRs). GRs have a role in normalizing stress-induced effects and promoting consolidation, while MRs are thought to be important in determining the threshold for activation of the hypothalamic-pituitary-adrenal (HPA) axis. We investigated the effects of MR blockade on HPA axis responses to stress and stress-induced changes in cognitive function. In a double-blind, placebo-controlled study, 64 healthy young men received 400 mg of the MR antagonist spironolactone or placebo. After 1.5 h, they were exposed to either a Trier Social Stress Test or a non-stressful control task. Responses to stress were evaluated by hormonal, subjective, and physiological measurements. Afterwards, selective attention, working memory, and long-term memory performance were assessed. Spironolactone increased basal salivary cortisol levels as well as cortisol levels in response to stress. Furthermore, spironolactone significantly impaired selective attention, but only in the control group. The stress group receiving spironolactone showed impaired working memory performance. By contrast, long-term memory was enhanced in this group. These data support a role of MRs in the regulation of the HPA axis under basal conditions as well as in response to stress. The increased availability of cortisol after spironolactone treatment implies enhanced GR activation, which, in combination with MR blockade, presumably resulted in a decreased MR/GR activation ratio. This condition influences both selective attention and performance in various memory tasks.

Demanding cognitive tasks are sometimes carried out under stressful conditions. Several studies indicate that whereas severe stress impairs performance, moderate stress can enhance cognitive performance. In this study, we investigated how moderate stress influences the neural systems supporting working memory. We embedded an N-back working memory task in a moderately stressful context, as indicated by our physiological stress measures, and probed phasic and tonic human brain activity using two fMRI-techniques: conventional blood oxygen level dependent fMRI and arterial spin labeling (ASL). The results showed that the stress induction, as compared to the neutral control condition, led to slightly faster reaction times without changes in accuracy. In general, working memory processing was associated with increased activity in a frontoparietal network and reduced activity in the medial temporal lobe (MTL). The stress induction led to enhanced reduction of phasic MTL responses, specifically the hippocampus and amygdala. In addition, ASL showed that stress increased tonic amygdala activity, while tonic hippocampal activity was unaffected. These findings suggest that the influence of stress on MTL deactivation during working memory processing is task-related rather than a general consequence of the stressful state. The temporal suspension of hippocampal processing in favor of more task relevant processes may allow subjects to maintain normal performance levels under moderate stress.

Miller (1956) summarized evidence that people can remember about seven chunks in short-term memory (STM) tasks. However, that number was meant more as a rough estimate and a rhetorical device than as a real capacity limit. Others have since suggested that there is a more precise capacity limit, but that it is only three to five chunks. The present target article brings together a wide variety of data on capacity limits suggesting that the smaller capacity limit is real. Capacity limits will be useful in analyses of information processing only if the boundary conditions for observing them can be carefully described. Four basic conditions in which chunks can be identified and capacity limits can accordingly be observed are: (1) when information overload limits chunks to individual stimulus items, (2) when other steps are taken specifically to block the recording of stimulus items into larger chunks, (3) in performance discontinuities caused by the capacity limit, and (4) in various indirect effects of the capacity limit. Under these conditions, rehearsal and long-term memory cannot be used to combine stimulus items into chunks of an unknown size; nor can storage mechanisms that are not capacity-limited, such as sensory memory, allow the capacity-limited storage mechanism to be refilled during recall. A single, central capacity limit averaging about four chunks is implicated along with other, noncapacity-limited sources. The pure STM capacity limit expressed in chunks is distinguished from compound STM limits obtained when the number of separately held chunks is unclear. Reasons why pure capacity estimates fall within a narrow range are discussed and a capacity limit for the focus of attention is proposed.

Acute stress impairs prefrontal cortex (PFC) function and has detrimental effects on working memory (WM) performance. Converging evidence from electrophysiological studies suggests a close link between WM processes and frontal theta (FT) activity (4-8 Hz). However, the effect of stress on WM-related FT activity has not been investigated yet. To shed light on this topic we acquired EEG data from 31 healthy male subjects who underwent a stressful and a neutral control condition. In both conditions, they performed an n-back WM task at two different difficulty levels. Our results showed that WM-related FT activity was decreased under stress. Behaviorally, we found performance impairments under stress in the difficult task condition that were related to FT decreases. Increased cortisol levels indicated a successful moderate stress induction. These findings indicate that FT is a potential neurobiological marker for intact PFC functioning during WM and further supports the recently made assumption that FT acts in the PFC to optimize performance.

Several brain areas show signal decreases during many different cognitive tasks in functional imaging studies, including the posterior cingulate cortex (PCC) and a medial frontal region incorporating portions of the medial frontal gyrus and ventral anterior cingulate cortex (MFG/vACC). It has been suggested that these areas are components in a default mode network that is engaged during rest and disengaged during cognitive tasks. This study investigated the functional connectivity between the PCC and MFG/vACC during a working memory task and at rest by examining temporal correlations in magnetic resonance signal levels between the regions. The two regions were functionally connected in both conditions. In addition, performance on the working memory task was positively correlated with the strength of this functional connection not only during the working memory task, but also at rest. Thus, it appears these regions are components of a network that may facilitate or monitor cognitive performance, rather than becoming disengaged during cognitive tasks. In addition, these data raise the possibility that the individual differences in coupling strength between these two regions at rest predict differences in cognitive abilities important for this working memory task.

Context: Postmenopausal estradiol therapy (ET) can reduce the stress response. However, it remains unclear whether such reductions can mitigate effects of stress on cognition. Objective: Investigate effects of ET on cortisol response to a physical stressor, cold pressor test (CPT), and whether ET attenuates stress effects on working memory. Design: Women completed the CPT or control condition across two sessions and subsequently completed a sentence span task. Setting: General community: Participants were recruited from the Early vs Late Intervention Trial with Estradiol (ELITE). Participants: ELITE participants (mean age = 66, standard deviation age = 6.8) in this study did not suffer from any major chronic illness or use medications known to affect the stress response or cognition. Interventions: Participants had received a median of randomized 4.7 years of estradiol (n = 21) or placebo (n = 21) treatment at time of participation in this study. Main Outcome Measures: Salivary cortisol and sentence span task performance. Results: Women assigned to estradiol exhibited blunted cortisol responses to CPT compared with placebo (P = 0.017) and lesser negative effects of stress on working memory (P = 0.048). Conclusions: We present evidence suggesting ET may protect certain types of cognition in the presence of stress. Such estrogenic protection against stress hormone exposure may prove beneficial to both cognition and the neural circuitry that maintains and propagates cognitive faculties.

The notion that stress plays a role in the etiology of psychotic disorders, especially schizophrenia, is longstanding. However, it is only in recent years that the potential neural mechanisms mediating this effect have come into sharper focus. The introduction of more sophisticated models of the interplay between psychosocial factors and brain function has expanded our opportunities for conceptualizing more detailed psychobiological models of stress in psychosis. Further, scientific advances in our understanding of adolescent brain development have shed light on a pivotal question that has challenged researchers; namely, why the first episode of psychosis typically occurs in late adolescence/young adulthood. In this paper, we begin by reviewing the evidence supporting associations between psychosocial stress and psychosis in diagnosed patients as well as individuals at clinical high risk for psychosis. We then discuss biological stress systems and examine changes that precede and follow psychosis onset. Next, research findings on structural and functional brain characteristics associated with psychosis are presented; these findings suggest that normal adolescent neuromaturational processes may go awry, thereby setting the stage for the emergence of psychotic syndromes. Finally, a model of neural mechanisms underlying the pathogenesis of psychosis is presented and directions for future research strategies are explored.

BACKGROUND: Anxiety is an aversive emotional state characterized by perceived uncontrollability and hypervigilance to threat that can frequently cause disruptions in higher-order cognitive processes like working memory. The attentional control theory (ACT) predicts that anxiety negatively affects the working memory system. DESIGN: This study tested the association between anxiety and working memory after the addition of stress and measured the glucocorticoid, cortisol. To better understand this relationship, we utilized a moderated mediation model. METHODS: Undergraduate students from a public university (N = 103) self-reported their anxiety levels. Participants first completed a short-term memory test. During and after a forehead cold pressor task (stress vs. control procedure) participants completed a working memory test. Salivary cortisol was taken at baseline and after the last working memory test. RESULTS: Overall, acute stress had no effect on working memory. However, we found that anxiety levels mediated the influence of condition (stressed vs. control) on working memory, but only among those individuals who had high cortisol levels after exposure to acute stress, supporting a moderated mediation model. CONCLUSIONS: These results imply that activation of the hypothalamic-pituitary-adrenal axis was necessary for working memory impairment in anxious individuals. These results provide support for the ACT.

Neural oscillations in the theta band (4-8 Hz) are prominent in the human electroencephalogram (EEG), and many recent electrophysiological studies in animals and humans have implicated scalp-recorded frontal midline theta (FMT) in working memory and episodic memory encoding and retrieval processes. However, the functional significance of theta oscillations in human memory processes remains largely unknown. Here, we review studies in human and animals examining how scalp-recorded FMT relates to memory behaviors and also their possible neural generators. We also discuss models of the functional relevance of theta oscillations to memory processes and suggest promising directions for future research.

Using event-related potentials (ERPs), we examined the time course of 39 healthy novice drivers during a blocked working memory task (numerical N-back) under acute social stress or control conditions, which were induced by the Trier Social Stress Task (TSST) or control procedure. Subjective measures were used to assess stress manipulation throughout the experiment. An elevated negative effect in response to a stress condition indicated a successful stress induction. The behavioral results showed that the stress group had a longer response time and larger differences in accuracy than the control group. On a neural level, the control group had larger P3 amplitude in the 1-back condition than in the 2-back condition; this load effect, however, disappeared in the stress group. These results revealed that acute social stress had a disruptive effect on both working memory behavioral performance and cognitive neural process. These findings provide us with a basis to understand the correlation between acute stress and cognitive processes of working memory at a cognitive neural level.

Stressful events activate the amygdala and a network of associated brain regions. Studies in both humans and rodents indicate that noradrenaline has a prominent role in this activation. Noradrenaline induces a hypervigilant state that helps to remember the event. This mnemonic effect is enhanced when the situation is so stressful that substantial amounts of corticosteroids are released and reach the amygdala. The combination of the two hormones leads to optimal strengthening of contacts and thus memory. Yet, rises in corticosteroid levels that are not precisely synchronized with noradrenaline release do not act synergistically but rather prevent or suppress the effect of noradrenaline. This dynamic interaction illustrates the adaptive and potentially protective capacity of corticosteroids regarding traumatic memories.

Stress is a strong modulator of memory function. However, memory is not a unitary process and stress seems to exert different effects depending on the memory type under study. Here, we explored the impact of social stress on different aspects of human memory, including tests for explicit memory and working memory (for neutral materials), as well as implicit memory (perceptual priming, contextual priming and classical conditioning for emotional stimuli). A total of 35 young adult male students were randomly assigned to either the stress or the control group, with stress being induced by the Trier Social Stress Test (TSST). Salivary cortisol levels were assessed repeatedly throughout the experiment to validate stress effects. The results support previous evidence indicating complex effects of stress on different types of memory: A pronounced working memory deficit was associated with exposure to stress. No performance differences between groups of stressed and unstressed subjects were observed in verbal explicit memory (but note that learning and recall took place within 1 h and immediately following stress) or in implicit memory for neutral stimuli. Stress enhanced classical conditioning for negative but not positive stimuli. In addition, stress improved spatial explicit memory. These results reinforce the view that acute stress can be highly disruptive for working memory processing. They provide new evidence for the facilitating effects of stress on implicit memory for negative emotional materials. Our findings are discussed with respect to their potential relevance for psychiatric disorders, such as post traumatic stress disorder.

The effects of various doses (40 microg/kg/hr, 300 microg/kg/hr, 600 microg/kg/hr or placebo) of hydrocortisone on tasks assessing working and declarative memory function were measured in 4 groups of 10 young men. During the infusion, participants were given an item-recognition working memory task, a paired-associate declarative memory task, and a continuous performance task used to control possible concomitant effects of corticosteroids on vigilance. The results revealed significant acute effects of the highest dose of hydrocortisone on working memory function, without any significant effect on declarative memory function or arousal-vigilance performance. These results suggest that working memory is more sensitive than declarative memory to the acute elevations of corticosteroids, which could explain the detrimental effects of corticosteroids on acquisition and consolidation of information, as reported in the literature.

BACKGROUND: Virtual reality (VR) is increasingly used to study and treat psychiatric disorders. Its fidelity depends in part on the extent to which the VR environment provides a convincing simulation, for example whether a putatively stressful VR situation actually produces a stress response. METHODS: We studied the stress response in 28 healthy men exposed either to a stressor VR elevator (which simulated travelling up the outside of a tall building and culminated in the participant being asked to step off the elevator platform), or to a control elevator. We measured psychological and physiological (salivary cortisol and alpha-amylase, blood pressure, pulse, skin conductance) stress indices. We also measured subsequent performance on the N-back task because acute stress has been reported to impact on working memory. RESULTS: Compared to participants in the control elevator, those in the external elevator had increases in skin conductance, pulse and subjective stress and anxiety ratings, altered heart rate variability, and a delayed rise in cortisol. N-back performance was unaffected. CONCLUSIONS: A putatively stressful VR elevator produces a physiological as well as a psychological stress response, supporting its use in the investigation and treatment of stress-related disorders, and its potential value as an experimental laboratory stressor.

BACKGROUND: Pre-clinical and clinical studies have shown acute stress may impair working memory and visuo-spatial ability. This study was designed to clarify the nature of stress-induced cognitive deficits in soldiers and how such deficits may contribute to operational or battlefield errors. METHODS: One hundred eighty-four Special Operations warfighters enrolled in Survival School completed pre-stress measures of dissociation and trauma exposure. Subjects were randomized to one of three assessment groups (Pre-stress, Stress, Post-stress) and were administered the Rey Ostereith Complex Figure (ROCF). All subjects completed post-stress measures of dissociation. RESULTS: ROCF copy and recall were normal in the Pre- and Post-stress groups. ROCF copy and recall were significantly impaired in the Stress Group. Stress group ROCF copy performance was piecemeal, and ROCF recall was impaired. Symptoms of dissociation were negatively associated with ROCF recall in the Stress group. Baseline dissociation and history of traumatic stress predicted cognitive impairment during stress. CONCLUSIONS: Stress exposure impaired visuo-spatial capacity and working memory. In rats, monkeys, and humans, high dopamine and NE turnover in the PFC induce deficits in cognition and spatial working memory. Improved understanding of stress-induced cognitive deficits may assist in identification of soldiers at risk and lead to the development of better countermeasures.

Stress and cortisol are known to impair memory retrieval of well-consolidated declarative material. The effects of cortisol on memory retrieval may in particular be due to glucocorticoid (GC) receptors in the hippocampus and prefrontal cortex (PFC). Therefore, effects of stress and cortisol should be observable on both hippocampal-dependent declarative memory retrieval and PFC-dependent working memory (WM). In the present study, it was tested whether psychosocial stress would impair both WM and memory retrieval in 20 young healthy men. In addition, the association between cortisol levels and cognitive performance was assessed. It was found that stress impaired WM at high loads, but not at low loads in a Sternberg paradigm. High cortisol levels at the time of testing were associated with slow WM performance at high loads, and with impaired recall of moderately emotional, but not of highly emotional paragraphs. Furthermore, performance at high WM loads was associated with memory retrieval. These data extend previous results of pharmacological studies in finding WM impairments after acute stress at high workloads and cortisol-related retrieval impairments.

Few studies have investigated the effect of an acute psychosocial stress paradigm on impaired attention and working memory in humans. Further, the duration of any stress-related cognitive impairment remains unclear. The aim of this study was to examine the effect of an acute psychosocial stress paradigm, the Trier Social Stress, on cognitive function in healthy volunteers. Twenty-three healthy male and female subjects were exposed to an acute psychosocial stress task. Physiological measures (salivary cortisol, heart rate and blood pressure) and subjective stress ratings were measured at baseline, in anticipation of stress, immediately post-stress and after a period of rest. A neuropsychological test battery including spatial working memory and verbal memory was administered at each time point. Acute psychosocial stress produced significant increases in cardiovascular and subjective measures in the anticipatory and post-stress period, which recovered to baseline after rest. Salivary cortisol steadily declined over the testing period. Acute psychosocial stress impaired delayed verbal recall, attention and spatial working memory. Attention remained impaired, and delayed verbal recall continued to decline after rest. Acute psychosocial stress is associated with an impairment of a broad range of cognitive functions in humans and with prolonged abnormalities in attention and memory.

We examined the relationship between acute stress and prefrontal-cortex (PFC) based working memory (WM) systems using behavioral (Experiment 1) and functional magnetic resonance imaging (fMRI; Experiment 2) paradigms. Subjects performed a delayed-response item-recognition task, with alternating blocks of high and low WM demand trials. During scanning, participants performed this task under three stress conditions: cold stress (induced by cold-water hand-immersion), a room temperature water control (induced by tepid-water hand-immersion), and no-water control (no hand-immersion). Performance was affected by WM demand, but not stress. Cold stress elicited greater salivary cortisol readings in behavioral subjects, and greater PFC signal change in fMRI subjects, than control conditions. These results suggest that, under stress, increases in PFC activity may be necessary to mediate cognitive processes that maintain behavioral organization.

Corticosteroids are important mediators of homeostasis and stress, and exert their effects via two transcription-factor receptors, mineralocorticoid receptor (MR) and glucocorticoid receptor (GR). Both receptors are expressed in the brain in a region-specific manner, and regulate neuroendocrine and behavioral functions. Stress during early development has been demonstrated to lead to long-term alterations in MR and GR levels and in the phenotypes that they mediate. To date, however, nearly all of this evidence has been obtained in rats, and there is actually no clear basis for extrapolation to other species. The current comparative review presents data, as available, on the following aspects of GR and MR gene expression in mouse and rat (Rodentia), tree shrew (Scandentia), common marmoset, squirrel monkey, rhesus macaque and human (Primates): (1) species-typical adult expression of MR mRNA and GR mRNA in hypothalamus, amygdala, hippocampus and neocortex; (2) species-typical neonate, infant, juvenile/adolescent and adult expression of MR mRNA and GR mRNA in hippocampus. (1) and (2) allow for identification of inter-species consistencies and differences in the relative levels of MR and GR expression across brain regions and ontogenetic stages. In addition, data are presented on (3) within-species inter-individual variation in MR and GR expression and causes thereof, including polymorphism and early life stress. Integrating the evidence in (1)-(3), it is noted that, should the expression levels of MR and GR at the time of early-life stress determine the latter's effects on the formers' long-term expression levels and functioning, then the long-term effects of early life stress on corticosteroid receptor expression and function will be species-, brain-region- and receptor-type-specific.

The present study aimed to investigate the subjective stress, salivary cortisol, and electrophysiological responses to psychological stress induced by a modified version of a mental arithmetic task. Fifteen participants were asked to estimate whether the multiplication product of two-decimal numbers was above 10 or not either with a time limit (the stress condition) or without a time limit (the control condition). The results showed that participants reported higher levels of stress, anxiety, and negative affect in the stress condition than they did in the control condition. Moreover, the salivary cortisol level continued to increase after the stress condition but exhibited a sharp decrease after the control condition. In addition, the electrophysiological data showed that the amplitude of the frontal-central N1 component was larger for the stress condition than it was for the control condition, while the amplitude of the frontal-central P2 component was larger for the control condition than it was for the stress condition. Our study suggests that the psychological stress characteristics of time pressure and social-evaluative threat caused dissociable effects on perception and on the subsequent attentional resource allocation of visual information.

We aimed to investigate the effect of mild acute psychological stress on attention processing by adopting a consecutive task paradigm. In each trial, a probe stimulus (left or right arrow) was presented immediately after a mental arithmetic task (psychological stressor). Participants were asked to estimate whether the product of a multiplication term was above 10 or not, either with (stress block) or without (control block) time pressure and social-evaluative threat. When the probe was presented, participants were asked to judge the direction of the arrows. Increased subjective stress and negative affect were found for the stress versus control trials. For the probe task, reaction times were faster in the stress block than in the control block. Event-related potentials locked to the arrows revealed that (a) fronto-central N1 was enhanced in the stress block compared to the control block. This finding might indicate that stress amplified processes of early perception and that vigilance and sensory intake were augmented. (b) fronto-central N2 was enhanced in the stress block compared to the control block. This finding might reflect increased effort to control selective attention in completing the probe task. (c) less positive P3 was evoked in the stress block than in the control block. This finding potentially reflects the fact that fewer attentional resources were engaged in processing the probe, or that the activity associated with the process of response evaluation was decreased. In sum, mild acute psychological stress exerts a dissociable effect on the neural subprocesses of attention.

BACKGROUND: Acute psychological stress impairs higher-order cognitive function such as working memory (WM). Similar impairments are seen in various psychiatric disorders that are associated with higher susceptibility to stress and with prefrontal cortical dysfunctions, suggesting that acute stress may play a potential role in such dysfunctions. However, it remains unknown whether acute stress has immediate effects on WM-related prefrontal activity. METHODS: Using functional magnetic resonance imaging (fMRI), we investigated neural activity of 27 healthy female participants during a blocked WM task (numerical N-back) while moderate psychological stress was induced by viewing strongly aversive (vs. neutral) movie material together with a self-referencing instruction. To assess stress manipulation, autonomic and endocrine, as well as subjective, measurements were acquired throughout the experiment. RESULTS: Successfully induced acute stress resulted in significantly reduced WM-related activity in the dorsolateral prefrontal cortex (DLPFC), and was accompanied by less deactivation in brain regions that are jointly referred to as the default mode network. CONCLUSIONS: This study demonstrates that experimentally induced acute stress in healthy volunteers results in a reduction of WM-related DLPFC activity and reallocation of neural resources away from executive function networks. These effects may be explained by supraoptimal levels of catecholamines potentially in conjunction with elevated levels of cortisol. A similar mechanism involving acute stress as a mediating factor may play an important role in higher-order cognitive deficits and hypofrontality observed in various psychiatric disorders.

Findings from neurophysiology have supported the view that visual working memory (WM) relies on modulation of activity in object-selective populations of neurons in inferior temporal cortex. Here, using event-related functional magnetic resonance imaging, we investigated whether similar mechanisms support human visual working memory encoding and maintenance processes. We identified regions in inferior temporal cortex that exhibited category-specific responses during perception of faces (fusiform face area [FFA]) or scenes (parahippocampal place area [PPA]) and investigated whether activity in these regions would be modulated by demands to actively encode and maintain faces and scenes. Results showed that independent of perceptual stimulation, the FFA and PPA exhibited greater encoding- and maintenance-related activity when their favored stimulus was relevant to the recognition task. In contrast, maintenance-related activity in the dorsolateral prefrontal cortex (PFC) was modulated by memory load, regardless of the type of information that was task relevant. These results are consistent with the view that visual working memory encoding and maintenance processes are implemented through modulation of inferior temporal activity by prefrontal cortex.

Exposure to an acute naturalistic stressor induces both psychological and physiological changes in humans. The two studies reported here explored the impact of exposure to an acute naturalistic stressor on state anxiety, working memory and HPA axis activation (salivary cortisol). In both experiments, ten healthy male participants were exposed to an acute naturalistic stressor, helicopter underwater evacuation training (HUET), and their physiological and behavioural responses before (first study) and after (second study) the stressor were compared to ten non-stressed controls. The results of both experiments showed that working memory performance was preserved during anticipation of an acute stressor, but impairments were observed immediately after stress exposure. Participants reported significantly higher state anxiety levels during anticipation and following stress exposure, whereas significant elevations in cortisol levels were only observed 25 min post exposure to stress, but not before or immediately after stress exposure. The results of both experiments demonstrated a dissociation between behavioural and biochemical measures and provided evidence for a dissociation of the effects of stress on cognitive and physiological measures depending on the time of testing, with cognitive impairments most evident following stress exposure.

Previous findings indicate that administration of abeta-adrenoceptor antagonist systemically blocks glucocorticoid impairment of memory retrieval. Here, we report that beta-adrenoceptor activation in the hippocampus and the basolateral complex of the amygdala (BLA) is implicated in the impairing effects of glucocorticoids on memory retrieval. The specific glucocorticoid receptor (GR) agonist 11beta,17beta-dihydroxy-6,21-dimethyl-17alpha-pregna-4,6-trien-20yn-3-one (RU 28362) (15 ng) infused into the hippocampus of male Sprague Dawley rats 60 min before water maze retention testing, 24 hr after training, impaired probe trial retention performance, as assessed by quadrant search time and initial latency to cross the platform location. Because we found previously that RU 28362 infused into the hippocampus does not affect water maze acquisition or immediate recall, the findings suggest that the GR agonist-induced retention impairment was attributable to a selective influence on long-term memory retrieval. Likewise, systemic injections of the beta1-adrenoceptor partial agonist xamoterol (3.0 or 10.0 mg/kg, s.c.) 60 min before the probe trial dose-dependently impaired retention performance. The beta-adrenoceptor antagonist propranolol (2.0 mg/kg) administered subcutaneously before retention testing did not affect retention performance alone, but blocked the memory retrieval impairment induced by concurrent intrahippocampal infusions of RU 28362. Pretest infusions of the beta1-adrenoceptor antagonist atenolol into either the hippocampus (1.25 microg in 0.5 microl) or the BLA (0.5 microg in 0.2 microl) also prevented the GR agonist-induced memory retrieval impairment. These findings suggest that glucocorticoids impair retrieval of long-term spatial memory by facilitating noradrenergic mechanisms in the hippocampus, and additionally, that norepinephrine-mediated BLA activity is critical in enabling hippocampal glucocorticoid effects on memory retrieval.

Stress has been shown to influence working memory. However, sex differences and the potential impact of stimulus emotionality have not received much attention. In a first experiment the effects of stress on a neutral working memory (WM) paradigm were tested in male and female participants (Experiment 1). Experiment 2 employed the same paradigm but used emotional stimuli. For this purpose, healthy participants were exposed either to a stressful (Trierer Social Stress Test (TSST)) or to a non-stressful control condition. Subsequently, WM performance in an n-back task was assessed. In Experiment 1, single digits were used as stimuli, while in Experiment 2 neutral and negative pictures were additionally employed. Salivary cortisol and Alpha-Amylase (sAA) were measured before and three times after the treatment as a marker of hypothalamus-pituitary-adrenal (HPA) axis- and sympathetic nervous system (SNS) activity. In both experiments, stress caused a substantial cortisol and sAA increase. For WM performance (response time) a stress by sex interaction was apparent. Stress enhanced performance in men, while impairing it in women. In both experiments stress had no effect on response accuracy. No modulating effect of the emotional quality of stimuli on n-back performance was observed (study 2). The results indicate that the effect of acute stress on n-back performance differs between the sexes. In contrast to long-term memory, the influence of stress on WM appears not to be modulated by the emotionality of the employed stimuli if stimuli are potential targets as it is the case in the n-back task.

In contrast to the substantial number of studies investigating the effects of stress on declarative memory, effects of stress on working memory have received less attention. We compared working memory (numerical n-back task with single digits) in 40 men exposed either to psychosocial stress (Trier Social Stress Test (TSST)) or a control condition. Task difficulty was varied using two conditions (2-back vs. 3-back). Salivary cortisol (as a marker of hypothalamus-pituitary-adrenal (HPA) activity) and salivary alpha-amylase (sAA as a marker of sympathetic nervous system (SNS) activity) were assessed immediately before and three times after the stress or control condition. As expected stress resulted in an increase in cortisol, sAA, and negative affect. Subjects exposed to stress showed significant working memory impairments in both workload conditions. The analysis of variance indicated a main effect of stress for reaction time as well as accuracy. In addition, for reaction time a stress-block interaction occurred. Follow up tests revealed that only during the first block at each level of difficulty performance was significantly impaired by stress. Thus, the effects of stress became smaller the longer the task was performed. Results provide further evidence for impaired working memory after acute stress and illustrate the time course of this phenomenon.

The current study investigated the effects of cold pressor stress (CPS) on 2 working memory (WM) tasks differing in the demand they put on maintenance and executive processing. For this purpose 72 healthy young men were exposed either to a stress group or a nonstressful control group. Subsequently, WM performance on the O-Span task (Turner & Engle, 1989) and the digit span task was assessed. Salivary cortisol was measured before and 2 times after the treatment as a marker of hypothalamus-pituitary-adrenal (HPA) axis activity. Results revealed a significant performance impairment of the O-Span and the digit span task backward in stressed subjects that correlated negatively with CPS-induced cortisol increases. Digit span forward was neither affected by CPS nor related to the ensuing cortisol increases. These results indicate that acute stress impairs WM performance for tasks requiring executive functions that operate on the stored material but not for WM tasks that only require maintenance.

Individuals are often unable to identify the second target (T2) of two when it is presented within 500 ms after the first target (T1). This

Posttraumatic stress disorder (PTSD) is associated with regional alterations in brain structure and function that are hypothesized to contribute to symptoms and cognitive deficits associated with the disorder. We present here the first systematic meta-analysis of neurocognitive outcomes associated with PTSD to examine a broad range of cognitive domains and describe the profile of cognitive deficits, as well as modifying clinical factors and study characteristics. This report is based on data from 60 studies totaling 4,108 participants, including 1,779 with PTSD, 1,446 trauma-exposed comparison participants, and 895 healthy comparison participants without trauma exposure. Effect-size estimates were calculated using a mixed-effects meta-analysis for 9 cognitive domains: attention/working memory, executive functions, verbal learning, verbal memory, visual learning, visual memory, language, speed of information processing, and visuospatial abilities. Analyses revealed significant neurocognitive effects associated with PTSD, although these ranged widely in magnitude, with the largest effect sizes in verbal learning (d = -.62), speed of information processing (d = -.59), attention/working memory (d = -.50), and verbal memory (d =-.46). Effect-size estimates were significantly larger in treatment-seeking than community samples and in studies that did not exclude participants with attention-deficit/hyperactivity disorder, and effect sizes were affected by between-group IQ discrepancies and the gender composition of the PTSD groups. Our findings indicate that consideration of neuropsychological functioning in attention, verbal memory, and speed of information processing may have important implications for the effective clinical management of persons with PTSD. Results are further discussed in the context of cognitive models of PTSD and the limitations of this literature.

Stress can fundamentally alter neural responses to incoming information. Recent research suggests that stress and anxiety shift the balance of attention away from a task-directed mode, governed by prefrontal cortex, to a sensory-vigilance mode, governed by the amygdala and other threat-sensitive regions. A key untested prediction of this framework is that stress exerts dissociable effects on different stages of information processing. This study exploited the temporal resolution afforded by event-related potentials to disentangle the impact of stress on vigilance, indexed by early perceptual activity, from its impact on task-directed cognition, indexed by later postperceptual activity in humans. Results indicated that threat of shock amplified stress, measured using retrospective ratings and concurrent facial electromyography. Stress also double-dissociated early sensory-specific processing from later task-directed processing of emotionally neutral stimuli: stress amplified N1 (184-236 ms) and attenuated P3 (316-488 ms) activity. This demonstrates that stress can have strikingly different consequences at different processing stages. Consistent with recent suggestions, stress amplified earlier extrastriate activity in a manner consistent with vigilance for threat (N1), but disrupted later activity associated with the evaluation of task-relevant information (P3). These results provide a novel basis for understanding how stress can modulate information processing in everyday life and stress-sensitive disorders.

The hormone cortisol is often believed to play a pivotal role in the effects of stress on human cognition. This meta-analysis is an attempt to determine the effects of acute cortisol administration on core executive functions. Drawing on both rodent and stress literatures, we hypothesized that acute cortisol administration would impair working memory and set-shifting but enhance inhibition. Additionally, because cortisol is thought to exert different nongenomic (rapid) and genomic (slow) effects, we further hypothesized that the effects of cortisol would differ as a function of the delay between cortisol administration and cognitive testing. Although the overall analyses were nonsignificant, after separating the rapid, nongenomic effects of cortisol from the slower, genomic effects of cortisol, the rapid effects of cortisol enhanced response inhibition, g+ = 0.113, p=.016, but impaired working memory, g+ = -0.315, p=.008, although these effects reversed over time. Contrary to our hypotheses, there was no effect of cortisol administration on set-shifting. Thus, although we did not find support for the idea that increases in cortisol influence set-shifting, we found that acute increases in cortisol exert differential effects on working memory and inhibition over time.

A growing body of research has indicated that acute stress can critically impact memory. However, there are a number of inconsistencies in the literature, and important questions remain regarding the conditions under which stress effects emerge as well as basic questions about how stress impacts different phases of memory. In this meta-analysis, we examined 113 independent studies in humans with 6,216 participants that explored effects of stress on encoding, postencoding, retrieval, or postreactivation phases of episodic memory. The results indicated that when stress occurred prior to or during encoding it impaired memory, unless both the delay between the stressor and encoding was very short and the study materials were directly related to the stressor, in which case stress improved encoding. In contrast, postencoding stress improved memory unless the stressor occurred in a different physical context than the study materials. When stress occurred just prior to or during retrieval, memory was impaired, and these effects were larger for emotionally valenced materials than neutral materials. Although stress consistently increased cortisol, the magnitude of the cortisol response was not related to the effects of stress on memory. Nonetheless, the effects of stress on memory were generally reduced in magnitude for women taking hormonal contraceptives. These analyses indicate that stress disrupts some episodic memory processes while enhancing others, and that the effects of stress are modulated by a number of critical factors. These results provide important constraints on current theories of stress and memory, and point to new questions for future research. (PsycINFO Database Record

Core executive functions such as working memory, inhibition, and cognitive flexibility are integral to daily life. A growing body of research has suggested that acute stress may impair core executive functions. However, there are a number of inconsistencies in the literature, leading to uncertainty about how or even if acute stress influences core executive functions. We addressed this by conducting a meta-analysis of acute stress effects on working memory, inhibition, and cognitive flexibility. We found that stress impaired working memory and cognitive flexibility, whereas it had nuanced effects on inhibition. Many of these effects were moderated by other variables, such as sex. In addition, we compared effects of acute stress on core executive functions to effects of cortisol administration and found some striking differences. Our findings indicate that stress works through mechanisms aside from or in addition to cortisol to produce a state characterized by more reactive processing of salient stimuli but greater control over actions. We conclude by highlighting some important future directions for stress and executive function research.

Psychosocial stress influences cognitive abilities, such as long-term memory retrieval. However, less is known about the effects of stress on cognitive flexibility, which is mediated by different neurobiological circuits and could thus be regulated by different neuroendocrine pathways. In this study, we randomly assigned healthy adults to an acute stress induction or control condition and subsequently assessed participants' cognitive flexibility using an open-source version of the Wisconsin Card Sort task. Drawing on work in rodents, we hypothesized that stress would have stronger impairing effects on cognitive flexibility in men than women. As predicted, we found that stress impaired cognitive flexibility in men but did not significantly affect women. Our results thus indicate that stress exerts sex-specific effects on cognitive flexibility in humans and add to the growing body of research highlighting the need to consider sex differences in effects of stress.

It is widely recognized that acute stress and associated glucocorticoid stress responses yield memory-enhancing effects when the memory consolidation phase is targeted, while impairing effects are generally found with regard to memory retrieval performance. While some evidence exists that the memory-enhancing effects of consolidation stress are modulated by time of day, no study to date has investigated whether stress-induced retrieval deficits are also prone to such time of day effects. To address this issue, participants (N=76) were exposed to a stressor or control condition before a retrieval test that probed for neutral and negative words learned 24h before. Results show that stress exposure resulted in impaired retrieval of both neutral and negative words, but that time of day did not moderate this effect. This memory-impairing effect was larger for negative than for neutral information, and was significantly associated with stress-induced cortisol responses. The current findings demonstrate the robustness of stress-induced retrieval deficits throughout the day, in particular for emotional memory material, and further underscore the importance of cortisol reactivity in impairing memory retrieval.

The present study investigated the effect of acute stress on working memory and memory for neutral, emotionally negative, and emotionally positive words in healthy undergraduates. Participants (N=60) were exposed to either the Trier Social Stress Test (stress group) or a non-stressful task (control group). Analyses of salivary cortisol samples taken throughout the study showed elevated glucocorticoid levels after the experimental manipulation in the stress group, but not in the control group. Recall performance was impaired in the stress group, but only so for neutral words. No differences between the stress and control group were found on working memory measures. For the stress group, digit span forward and digit span total scores were associated with correct recall of neutral words. All in all, this study lends further support to the notion that the memory effects of exposure to acute stress depend on the valence of the memory material.

Past studies have demonstrated that increases in cortisol secretion are associated with either enhancements or impairments of long-term memory, depending on the subprocess involved. However, working memory is generally studied as a unified system within the cortisol literature. The present study sought to determine if cortisol increases are positively associated with increases in performance in the encoding subprocess of working memory, and whether increases are positively or negatively associated with performance changes in the maintenance subprocess. Thirty-three young men (M = 19.4 years, SD = 0.89) participated in a change-detection task, consisting of a condition requiring encoding only and a condition requiring both encoding and maintenance. To elicit a cortisol response, participants completed the Trier Social Stress Test (TSST) between two administrations of the task. Cardiovascular measurements and saliva samples were obtained before the TSST (T1), and mid-way between blocks of the second administration of the change-detection task (T2), to measure autonomic and cortisol responses to the TSST evident during the second change-detection task. Cortisol increases between T1 and T2 were positively correlated with both encoding (r(32) = 0.503, p = 0.003) and maintenance (r(32) = 0.463, p = 0.007) performance. This is a novel finding as previous studies have shown an impairing effect of cortisol on working memory. The positive relation between cortisol and working memory has likely been obscured in previous tasks, which did not examine these specific subprocesses in isolation from each other. The beneficial role of cortisol in the stress response is discussed.

Complaints of stress are common in modern life. Psychological stress is a major cause of lifestyle-related issues, contributing to poor quality of life. Chronic stress impedes brain function, causing impairment of many executive functions, including working memory, decision making and attentional control. The current study sought to describe newly developed stress mitigation techniques, and their influence on autonomic and endocrine functions. The literature search revealed that the most frequently studied technique for stress mitigation was biofeedback (BFB). However, evidence suggests that neurofeedback (NFB) and noninvasive brain stimulation (NIBS) could potentially provide appropriate approaches. We found that recent studies of BFB methods have typically used measures of heart rate variability, respiration and skin conductance. In contrast, studies of NFB methods have typically utilized neurocomputation techniques employing electroencephalography, functional magnetic resonance imaging and near infrared spectroscopy. NIBS studies have typically utilized transcranial direct current stimulation methods. Mitigation of stress is a challenging but important research target for improving quality of life.

The human stress response has been characterized, both physiologically and behaviorally, as

Working memory (WM) is the ability to keep a limited amount of information

BACKGROUND: Pediatric ADHD is associated with impairments in working memory, but these deficits often go undetected when using clinic-based tests such as digit span backward. AIMS: The current study pilot-tested minor administration/scoring modifications to improve digit span backward's construct and predictive validities in a well-characterized sample of children with ADHD. METHODS AND PROCEDURES: WISC-IV digit span was modified to administer all trials (i.e., ignore discontinue rule) and count digits rather than trials correct. Traditional and modified scores were compared to a battery of criterion working memory (construct validity) and academic achievement tests (predictive validity) for 34 children with ADHD ages 8-13 (M=10.41; 11 girls). OUTCOMES AND RESULTS: Traditional digit span backward scores failed to predict working memory or KTEA-2 achievement (allns). Alternate administration/scoring of digit span backward significantly improved its associations with working memory reordering (r=.58), working memory dual-processing (r=.53), working memory updating (r=.28), and KTEA-2 achievement (r=.49). CONCLUSIONS AND IMPLICATIONS: Consistent with prior work, these findings urge caution when interpreting digit span performance. Minor test modifications may address test validity concerns, and should be considered in future test revisions. Digit span backward becomes a valid measure of working memory at exactly the point that testing is traditionally discontinued.

OBJECTIVE: Several studies have shown that glucocorticoids can impair declarative memory retrieval and working memory (WM) performance. The aim of the present study was to investigate the impact of a high dose of hydrocortisone on WM, as well as to examine the effects of cortisol suppression via treatment with a high dose of dexamethasone (DEX). We hypothesized that hydrocortisone treatment results in an impaired cognitive function compared with placebo. We further expected that dexamethasone treatment is also followed by cognitive impairment, due to the hypothesis that very low levels of cortisol are also associated with alterations in memory performance. METHODS: In a placebo-controlled study with a within-subject design, 16 healthy volunteers received placebo or 120 mg of hydrocortisone (two boluses of 60 mg) directly before neuropsychological testing or 4 mg of DEX the day before testing. RESULTS: We did not find any effect of hydrocortisone on WM and cognitive flexibility, even though cortisol levels were high at the time of testing. Furthermore, we did not find any effect of DEX treatment on WM and reaction time in a cognitive flexibility test. However, cognitive flexibility was negatively correlated with adrenocorticotropin (ACTH) in the DEX condition. CONCLUSIONS: Our results found no clear effect of hydrocortisone and dexamethasone treatment on WM. These results emphasize the need for further research on the association between hypothalamic-pituitary-adrenal axis activity and cognition. These studies should investigate the hypotheses of dose-dependent associations in more detail and should also include analyses on ACTH and cognition.

Working memory processes are associated with the dorsolateral prefrontal cortex (dlPFC). Prior research using proton functional magnetic resonance spectroscopy ((1)H fMRS) observed significant dlPFC glutamate modulation during letter 2-back performance, indicative of working memory-driven increase in excitatory neural activity. Acute stress has been shown to impair working memory performance. Herein, we quantified dlPFC glutamate modulation during working memory under placebo (oral lactose) and acute stress conditions (oral yohimbine 54 mg + hydrocortisone 10 mg). Using a double-blind, randomized crossover design, participants (N = 19) completed a letter 2-back task during left dlPFC (1)H fMRS acquisition (Brodmann areas 45/46; 4.5cm(3)). An automated fitting procedure integrated with LCModel was used to quantify glutamate levels. Working memory-induced glutamate modulation was calculated as percentage change in glutamate levels from passive visual fixation to 2-back levels. Results indicated acute stress significantly attenuated working memory-induced glutamate modulation and impaired 2-back response accuracy, relative to placebo levels. Follow-up analyses indicated 2-back performance significantly modulated glutamate levels relative to passive visual fixation during placebo but not acute stress. Biomarkers, including blood pressure and saliva cortisol, confirmed that yohimbine + hydrocortisone dosing elicited a significant physiological stress response. These findings support a priori hypotheses and demonstrate that acute stress impairs dlPFC function and excitatory activity. This study highlights a neurobiological mechanism through which acute stress may contribute to psychiatric dysfunction and derail treatment progress. Future research is needed to isolate noradrenaline vs. cortisol effects and evaluate anti-stress medications and/or behavioral interventions.

The physiological stress system and the circadian clock system communicate with each other at different signaling levels. The steroid hormone cortisol, the end-effector of the hypothalamus-pituitary-adrenal axis, is released in response to stress and acts as a mediator in circadian rhythms. We determined the effect of escalating cortisol doses on the expression of PERIOD genes (PER1, PER2 and PER3) in healthy subjects and analyzed whether the glucocorticoid receptor (GR) is involved in the cortisol-mediated PERIOD gene expression. Forty participants (50% males and 50% females) were randomly assigned to groups receiving a saline placebo solution or 3 mg, 6 mg, 12 mg and 24 mg of hydrocortisone. Blood was drawn every 15 min to measure quantitative gene expression of PER1, PER2 and PER3. A potential role of the GR was determined by an ex vivo study stimulating whole blood with hydrocortisone and RU486 (a GR antagonist). As a result, moderate doses of hydrocortisone produced an acute and temporary induction of PER1 and PER3 mRNA levels, whereas PER2 was not responsive to the hormone administration. The cortisol-dependent induction of PER1 was blocked by the GR antagonist in whole blood after treatment with hydrocortisone and RU486 ex vivo. In conclusion, acute pharmacological stress modulated the expression of PER1 and PER3 in whole blood temporarily in our short-term sampling design, suggesting that these circadian genes mediate stable molecular mechanisms in the periphery.

Sex is considered a moderating factor in the relationship between stress and cognitive performance. However, sex differences and the impact of cognitive stress appraisal on working memory performance have not received much attention. The aim of this study was to investigate the role of physiological responses (heart rate and salivary cortisol) and cognitive stress appraisal in Working Memory (WM) performance in males and females. For this purpose, we subjected a comparable number of healthy young adult males (N=37) and females (N=45) to a modified version of the Trier Social Stress Test (TSST), and we evaluated WM performance before and after the stress task. Females performed better on attention and maintenance after the TSST, but males did not. Moreover, we found that attention and maintenance performance presented a negative relationship with cortisol reactivity in females, but not in males. Nevertheless, we observed that only the females who showed a cortisol decrease after the TSST performed better after the stress task, whereas females and males who showed an increase or no change in cortisol levels, and males who showed a cortisol decrease, did not change their performance over time. In females, we also found that the global indexes of cognitive stress appraisal and cognitive threat appraisal were negatively related to attention and maintenance performance, whereas the Self-concept of Own Competence was positively related to it. However, these relationships were not found in males.

Stress is associated with relapse to drugs after abstinence, but the mechanisms for this association are unclear. One mechanism may be that stress enhances abstinent addicts' recall of memories of drugs as stress relievers. This study assessed the effects of stress on free recall and cued recall of 10 heroin-related and 10 neutral words learned 24 h earlier by 102 abstinent heroin addicts. These participants were randomly assigned to three experiments that also assessed attention and working memory. Experiment 1 used a psychosocial stressor (Trier social stress test (TSST)) before testing for recall of heroin-related words. Experiment 2 added administration of the beta-adrenoceptor antagonist propranolol 1 h before the psychosocial stressor. Experiment 3 added administration of either cortisol with propranolol, cortisol alone, or propranolol alone 1 h before word recall to determine whether stress enhancement of heroin-related word recall required noradrenergic-glucocorticoid interactions. We found that free recall of heroin-related words in abstinent addicts was enhanced after stress or cortisol administration when compared with a non-stress condition or placebo, respectively, whereas these interventions had no effect on neutral word recall. beta-adrenergic blockade blocked the enhancing effect of stress or cortisol on free recall of heroin-related words. Neither stress nor cortisol affected cued recall, attention, or working memory. The potential of beta-adrenergic blockade to reduce or block stress-induced enhancement of drug-related memory retrieval may be relevant to preventing stress-induced relapse in abstinent heroin addicts.

Behavioral observations suggest that multiple sensory elements can be maintained for a short time, forming a perceptual buffer which fades after a few hundred milliseconds. Only a subset of this perceptual buffer can be accessed under top-down control and broadcasted to working memory and consciousness. In turn, single-cell studies in awake-behaving monkeys have identified two distinct waves of response to a sensory stimulus: a first transient response largely determined by stimulus properties and a second wave dependent on behavioral relevance, context and learning. Here we propose a simple biophysical scheme which bridges these observations and establishes concrete predictions for neurophsyiological experiments in which the temporal interval between stimulus presentation and top-down allocation is controlled experimentally. Inspired in single-cell observations, the model involves a first transient response and a second stage of amplification and retrieval, which are implemented biophysically by distinct operational modes of the same circuit, regulated by external currents. We explicitly investigated the neuronal dynamics, the memory trace of a presented stimulus and the probability of correct retrieval, when these two stages were bracketed by a temporal gap. The model predicts correctly the dependence of performance with response times in interference experiments suggesting that sensory buffering does not require a specific dedicated mechanism and establishing a direct link between biophysical manipulations and behavioral observations leading to concrete predictions.