Drawbacks to Strengthening Neural Salience Encoding: A Link Between Cortisol and Risky Drinking.

Emotionally salient experiences are encoded and remembered more strongly, an effect that can be amplified by hormones like cortisol. Such memories can in turn profoundly influence later behavior. However, little is known about the link between amplified salience encoding and subsequent behavior. This pathway may be particularly important for risky alcohol drinking, which has been linked to sensitized salience responses, memory, and cortisol. To test this possibility, we integrated pharmacology using a double-blind cross-over design with fMRI, cognitive, and motivation assays across a range of healthy male and female social drinkers. As anticipated, cortisol enhanced memory for salient alcohol-related events; critically, this bias was in turn associated with later alcohol motivation. Increased alcohol motivation was particularly pronounced in more susceptible risky drinkers, for whom cortisol enhanced brain salience responses to alcohol. These sensitized salience responses predicted both memory biases and alcohol motivation. Together, these findings reveal maladaptive consequences of enhanced salience encoding.

Fibrous MXene Synapse-Based Biomimetic Tactile Nervous System for Multimodal Perception and Memory.

Biomimetic tactile nervous system (BTNS) inspired by organisms has motivated extensive attention in wearable fields due to its biological similarity, low power consumption, and perception-memory integration. Though many works about planar-shape BTNS are developed, few researches could be found in the field of fibrous BTNS (FBTNS) which is superior in terms of strong flexibility, weavability, and high-density integration. Herein, a FBTNS with multimodal sensibility and memory is proposed, by fusing the fibrous poly lactic acid (PLA)/Ag/MXene/Pt artificial synapse and MXene/EMIMBF4 ionic conductive elastomer. The proposed FBTNS can successfully perceive external stimuli and generate synaptic responses. It also exhibits a short response time (23 ms) and low set power consumption (17 nW). Additionally, the proposed device demonstrates outstanding synaptic plasticity under both mechanical and electrical stimuli, which can simulate the memory function. Simultaneously, the fibrous devices are embedded into textiles to construct tactile arrays, by which biomimetic tactile perception and temporary memory functions are successfully implemented. This work demonstrates the as-prepared FBTNS can generate biomimetic synaptic signals to serve as artificial feeling signals, it is thought that it could offer a fabric electronic unit integrating with perception and memory for Human-Computer interaction, and has great potential to build lightweight and comfortable Brain-Computer interfaces.

Behavioral and brain- transcriptomic synchronization between the two opponents of a fighting pair of the fish Betta splendens.

Conspecific male animals fight for resources such as food and mating opportunities but typically stop fighting after assessing their relative fighting abilities to avoid serious injuries. Physiologically, how the fighting behavior is controlled remains unknown. Using the fighting fish Betta splendens, we studied behavioral and brain-transcriptomic changes during the fight between the two opponents. At the behavioral level, surface-breathing, and biting/striking occurred only during intervals between mouth-locking. Eventually, the behaviors of the two opponents became synchronized, with each pair showing a unique behavioral pattern. At the physiological level, we examined the expression patterns of 23,306 brain transcripts using RNA-sequencing data from brains of fighting pairs after a 20-min (D20) and a 60-min (D60) fight. The two opponents in each D60 fighting pair showed a strong gene expression correlation, whereas those in D20 fighting pairs showed a weak correlation. Moreover, each fighting pair in the D60 group showed pair-specific gene expression patterns in a grade of membership analysis (GoM) and were grouped as a pair in the heatmap clustering. The observed pair-specific individualization in brain-transcriptomic synchronization (PIBS) suggested that this synchronization provides a physiological basis for the behavioral synchronization. An analysis using the synchronized genes in fighting pairs of the D60 group found genes enriched for ion transport, synaptic function, and learning and memory. Brain-transcriptomic synchronization could be a general phenomenon and may provide a new cornerstone with which to investigate coordinating and sustaining social interactions between two interacting partners of vertebrates.

Acute physical exercise promotes the consolidation of emotional material.

Physical exercise can improve cognitive functions and promote learning and memory, especially when performed in close temporal proximity to the encoding of information. This benefit may occur due to circulating stress hormones released in response to acute exercise. When administered after encoding, acute stress typically enhances the consolidation of emotional stimuli. However, whether acute exercise also selectively modulates emotional memories remains to be explored. Likewise, the potential role of sex in moderating these effects has not been addressed so far. Here, we tested whether a single bout of aerobic exercise after learning boosts the consolidation and thus long-term memory for emotional versus neutral visuospatial stimuli. Healthy men and women learned an object-location task and subsequently were exposed to a vigorous-treadmill running task or control intervention. Memory was assessed 24 h later. Acute exercise significantly increased heart rate and salivary cortisol in both sexes and selectively facilitated the consolidation of emotional stimuli. In particular, we found improved memory for negative items in women and better recall of positive items in men following exercise exposure. This memory benefit was positively related to the increase in heart rate and cortisol in both men and women, suggesting that the favorable effects of acute exercise on emotional memory may be mediated via a co-activation of the sympathetic nervous system and the hypothalamus-pituitary-adrenocortical axis. Our findings thereby provide first evidence for the improvement of emotional memory consolidation by acute physical exercise that appears to rely on similar neuroendocrine mechanisms as psychosocial stressors. Given that exercise is healthy, cost-effective and practical in nature, it constitutes an ideal behavioral intervention strategy for boosting memory in clinical and educational settings alike.

Use of the birth control pill affects stress reactivity and brain structure and function.

Millions of women worldwide use oral contraceptives (i.e., birth control pill; OCs), often starting during puberty/adolescence; however, it is unknown how OC use during this critical period of development affects the brain, especially with regard to emotional working memory. Here, we examined stress reactivity, and brain structure and function in OC users using the Trier Social Stress Test and structural and functional magnetic resonance imaging (MRI). Our results show that OC use during puberty/adolescence gives rise to a blunted stress response and alters brain activation during working memory processing. OC use, in general, is also linked to increased prefrontal brain activation during working memory processing for negatively arousing stimuli. OC use is also related to significant structural changes in brain regions implicated in memory and emotional processing. Together, these findings highlight that OC use induces changes to brain structure and function and alters stress reactivity. These findings may provide a mechanistic insight for the increased vulnerability to mood-related mental illness in women after OC use.

Reconsolidation impairment of reward memory by stimulating stress response.

Research in memory reconsolidation has raised hope for new treatment options of persistent psychiatric disorders like substance dependence and post-traumatic stress disorder (PTSD). While animal research showed successful memory modification by interfering with reconsolidation, human research requires less invasive techniques. In our pilot study, we aimed to reduce appetitive memory reconsolidation of a newly acquired reward memory by exerting a stressor. Thirty healthy participants were randomly assigned to two groups performing a monetary reward paradigm at a personal computer. Day 1 was considered to allow for memory acquisition; on day 2, the experimental group was exposed to a frightening stimulus in the reconsolidation window; and day 3 again served to determine reward memory effects. Measures of reward memory were reaction times to reward announcing stimuli (ie, showing instrumental behavior), actual reward gained, and electrodermal response as a measure for reward anticipation. We found significantly smaller reaction time improvements to reward stimuli over time in the experimental group, as well as reduced achievements in monetary reward. Electrodermal response to reward announcing stimuli was lower in the experimental group after intervention, whereas it was higher in the untreated group. Thus, we argue in favor of the reconsolidation hypothesis, assuming our intervention had successfully interfered with the reconsolidation process. This points towards future treatment options that interfere with an addiction memory.

Determining the biological associates of acute cold pressor post-encoding stress effects on human memory: The role of salivary interleukin-1ß.

Stress generally hurts many aspects of memory, but an interesting finding to emerge from the stress and memory literature is that stress that occurs shortly after learning (i.e., post-encoding stress) usually benefits memory. Although this effect is well established, the biological mechanisms underpinning this effect are not-especially in humans. We addressed this gap in the present study by collecting saliva samples from 80 participants who were randomized to a post-encoding stress (i.e., cold pressor for 3 min) or control task (i.e., warm water for 3 min) and 48 h later completed a recognition memory task. Saliva was collected both prior to and 15 min after the offset of (18 min after the onset of) the stress/control manipulation. Drawing on animal and human work, we examined how five stress-responsive biomarkers-cortisol, salivary α-amylase, progesterone, estradiol, and the proinflammatory cytokine interleukin (IL)-1ß, all assessed in saliva-related to the effects of stress on memory. We found that stress enhanced recollection of negative images and that these effects were selectively related to salivary IL-1ß. Moreover, we found that the beneficial effects of stress on memory were statistically mediated by salivary IL-1ß. We found no robust associations-either linear or quadratic-between memory and any other biomarker, nor did we find significant interactions between biomarkers in predicting memory. These results suggest that immune system activity indexed by salivary IL-1ß may play an important role in contributing to post-encoding stress effects on human memory.

Prenatal cortisol modifies the association between maternal trauma history and child cognitive development in a sex-specific manner in an urban pregnancy cohort.

Women's experience of trauma may cause lifelong alterations in physiological stress regulation, which can be transmitted to offspring in utero. We investigated, in a prospective pregnancy cohort, associations among maternal lifetime interpersonal trauma (IPT) history, prenatal cortisol dysregulation, and children's memory domains. Sex-specific effects were also explored. Pregnant women were enrolled from Brigham & Women's Hospital and affiliated clinics near Boston, MA, in 2002-2007. IPT was assessed with the Revised Conflict Tactics Scale, short form. Salivary cortisol was measured at five time points on each of three days in one week at 29.0 ± 5.1 weeks gestation, and morning rise and diurnal slope were calculated. The Wide Range Assessment of Memory & Learning, 2nd Edition was administered at 6.5 ± 1.0 years and scores were generated for general memory and three sub-domains: verbal, visual, and attention/concentration. In total, 258 maternal-child dyads provided memory and IPT and/or cortisol data. IPT was positively associated with verbal memory in boys (ß ± SE: 4.6 ± 2.6) and inversely associated with visual memory score in girls (-6.5 ± 3.2). IPT did not predict prenatal cortisol, but prenatal cortisol modified the association between IPT history and child memory in varying coefficient models allowing for non-linear effect modification. The strongest evidence of interaction was for visual memory in boys: IPT history was associated with poorer visual memory only in those with flatter prenatal diurnal slope (interaction p = .005). Maternal lifetime IPT that leads to prenatal HPA dysregulation may have consequences for child memory, more so than either trauma or elevated cortisol alone. Boys may be more vulnerable to effects. Sex- and timing-specific effects require further investigation.

Estrogen receptor-alpha knockouts and maternal memory in nulliparous rats.

The current study investigated the role of estrogen receptor alpha (Esr1) in maternal memory in rats, comparing the induction and retention responses of Esr1 knockout (KO) and wild type (WT) nulliparous rats towards foster pups. Thirty days after completion of induction testing, subjects were tested for the retention of maternal care in their home cage and then for maternal behaviors in a novel cage. Both WT and Esr1 KO females displayed similar latencies to respond to foster young during the initial induction testing. Likewise, reinduction latencies to display full maternal responsiveness were similar in the Esr1 KO and WT groups during maternal memory testing in the home cage. However, in the novel cage testing WT subjects displayed modest modifications in maternal care. WT females had shorter latencies to first retrieve and mouth a test pup. These findings suggest that while Esr1 does not appear to affect the establishment of maternal care or the display of maternal memory, it may modulate aspects of pup-directed behaviors associated with the reinduction of maternal care in female rats.

Cortisol and trait anxiety as relevant factors involved in memory performance in people with drug-resistant epilepsy.

People with drug-resistant epilepsy are exposed to unpredictable and uncontrollable seizures, which can be considered as a chronic stress condition. Additionally, these patients present memory deficits and a high prevalence of depression and anxiety. Cortisol, the main stress hormone, has a modulatory role on memory in healthy individuals and patients with emotional disorders, but its role in memory and emotional processes remains unclear in people with epilepsy. This study analyzes the differences in cortisol levels in people with epilepsy with high and low memory performance, and the relationships among cortisol levels, epilepsy-related factors, memory, anxiety, and depression. Fifty-two adults with drug-resistant epilepsy underwent a neuropsychological evaluation, in which nine saliva samples were collected to analyze the ability of the hypothalamic-pituitary-adrenal axis to descend in accordance with the circadian rhythm. Cortisol area under the curve (AUC) was computed to study the global cortisol changes. Patients with low immediate and delayed memory performance and left-hemisphere focus showed higher cortisol levels. Additionally, patients with low memory scores had higher cortisol AUC, and therefore slower declining levels in the afternoon. Memory performance was negatively related to the cortisol AUC and trait anxiety, being both reliable predictors of memory performance, especially in patients with left-hemisphere focus. These results suggest that memory deficits in people with drug-resistant epilepsy may be influenced by exposure to cortisol derived from chronic stress. Additionally, trait anxiety could contribute to increasing the vulnerability to stress.

Stress leads to aberrant hippocampal involvement when processing schema-related information.

Prior knowledge, represented as a mental schema, has critical impact on how we organize, interpret, and process incoming information. Recent findings indicate that the use of an existing schema is coordinated by the medial prefrontal cortex (mPFC), communicating with parietal areas. The hippocampus, however, is crucial for encoding schema-unrelated information but not for schema-related information. A recent study indicated that stress mediators may affect schema-related memory, but the underlying neural mechanisms are currently unknown. Here, we thus tested the impact of acute stress on neural processing of schema-related information. We exposed healthy participants to a stress or control manipulation before they processed, in the MRI scanner, words related or unrelated to a preexisting schema activated by a specific cue. Participants' memory for the presented material was tested 3-5 d after encoding. Overall, the processing of schema-related information activated the mPFC, the precuneus, and the angular gyrus. Stress resulted in aberrant hippocampal activity and connectivity while participants processed schema-related information. This aberrant engagement of the hippocampus was linked to altered subsequent memory. These findings suggest that stress may interfere with the efficient use of prior knowledge during encoding and may have important practical implications, in particular for educational settings.

A Deletion Variant of the α2b-Adrenoceptor Modulates the Stress-Induced Shift from "Cognitive" to "Habit" Memory.

Stress induces a shift from hippocampus-based "cognitive" toward dorsal striatum-based "habitual" learning and memory. This shift is thought to have important implications for stress-related psychopathologies, including post-traumatic stress disorder (PTSD). However, there is large individual variability in the stress-induced bias toward habit memory, and the factors underlying this variability are completely unknown. Here we hypothesized that a functional deletion variant of the gene encoding the α2b-adrenoceptor (ADRA2B), which has been linked to emotional memory processes and increased PTSD risk, modulates the stress-induced shift from cognitive toward habit memory. In two independent experimental studies, healthy humans were genotyped for the ADRA2B deletion variant. After a stress or control manipulation, participants completed a dual-solution learning task while electroencephalographic (Study I) or fMRI measurements (Study II) were taken. Carriers compared with noncarriers of the ADRA2B deletion variant exhibited a significantly reduced bias toward habit memory after stress. fMRI results indicated that, whereas noncarriers of the ADRA2B deletion variant showed increased functional connectivity between amygdala and putamen after stress, this increase in connectivity was absent in carriers of the deletion variant, who instead showed overall enhanced connectivity between amygdala and entorhinal cortex. Our results indicate that a common genetic variation of the noradrenergic system modulates the impact of stress on the balance between cognitive and habitual memory systems, most likely via altered amygdala orchestration of these systems.SIGNIFICANCE STATEMENT Stressful events have a powerful effect on human learning and memory. Specifically, accumulating evidence suggests that stress favors more rigid dorsal striatum-dependent habit memory, at the expense of flexible hippocampus-dependent cognitive memory. Although this shift may have important implications for understanding mental disorders, such as post-traumatic stress disorder, little is known about the source of individual differences in the sensitivity for the stress-induced bias toward habit memory. We report here that a common genetic variation of the noradrenergic system, a known risk factor for post-traumatic stress disorder, modulates the stress-induced shift from cognitive to habit memory, most likely through altered crosstalk between the hippocampus and dorsal striatum with the amygdala, a key structure in emotional memory.

The absence of maternal pineal melatonin rhythm during pregnancy and lactation impairs offspring physical growth, neurodevelopment, and behavior.

Maternal melatonin provides photoperiodic information to the fetus and thus influences the regulation and timing of the offspring's internal rhythms and preparation for extra-uterine development. There is clinical evidence that melatonin deprivation of both mother and fetus during pregnancy, and of the neonate during lactation, results in negative long-term health outcomes. As a consequence, we hypothesized that the absence of maternal pineal melatonin might determine abnormal brain programming in the offspring, which would lead to long-lasting implications for behavior and brain function. To test our hypothesis, we investigated in rats the effects of maternal melatonin deprivation during gestation and lactation (MMD) to the offspring and the effects of its therapeutic replacement. The parameters evaluated were: (1) somatic, physical growth and neurobehavioral development of pups of both sexes; (2) hippocampal-dependent spatial learning and memory of the male offspring; (3) adult hippocampal neurogenesis of the male offspring. Our findings show that MMD significantly delayed male offspring's onset of fur development, pinna detachment, eyes opening, eruption of superior incisor teeth, testis descent and the time of maturation of palmar grasp, righting reflex, free-fall righting and walking. Conversely, female offspring neurodevelopment was not affected. Later on, male offspring show that MMD was able to disrupt both spatial reference and working memory in the Morris Water Maze paradigm and these deficits correlate with changes in the number of proliferative cells in the hippocampus. Importantly, all the observed impairments were reversed by maternal melatonin replacement therapy. In summary, we demonstrate that MMD delays the appearance of physical features, neurodevelopment and cognition in the male offspring, and points to putative public health implications for night shift working mothers.

Neurocognitive, emotional and neuroendocrine correlates of exposure to sexual assault in women.

BACKGROUND: Survivors of sexual assault are vulnerable to long-term negative psychological and physical health outcomes, but few studies have investigated changes in cognition, emotional processing and brain function in the early stages after sexual assault. We used a multimodal approach to identify the cognitive and emotional correlates associated with sexual assault in women. METHODS: Twenty-seven female survivors of sexual assault were included within 4 weeks of the traumatic event, and they were compared with 20 age-matched controls. Participants underwent functional MRI while performing cognitive/emotional tasks (n-back, emotional go/no-go, mental imagery). We also measured diurnal salivary cortisol and conducted neuropsychological assessments of attention and memory abilities. RESULTS: Relative to the control group, the survivor group had lower levels of morning cortisol and showed attentional deficits. We observed no between-group differences in brain activation during the n-back or mental imagery tasks. During the emotional go/no-go task, however, the survivor group showed a lack of deactivation in the dorsal anterior cingulate cortex when processing emotional material, relative to neutral material. Exploratory analyses in the survivor group indicated that symptom severity was negatively associated with cerebellar activation when positive emotional (happy) content interfered with response inhibition, and positively associated with cerebellar activation when thinking of positive (happy) memories. LIMITATIONS: The small sample size was the main limitation of this study. CONCLUSION: Dysfunctions in the dorsal anterior cingulate cortex and the cerebellum may represent early functional brain modifications that alter higher cognitive processes when emotional material is involved.

Stress as a mnemonic filter: Interactions between medial temporal lobe encoding processes and post-encoding stress.

Acute stress has been shown to modulate memory for recently learned information, an effect attributed to the influence of stress hormones on medial temporal lobe (MTL) consolidation processes. However, little is known about which memories will be affected when stress follows encoding. One possibility is that stress interacts with encoding processes to selectively protect memories that had elicited responses in the hippocampus and amygdala, two MTL structures important for memory formation. There is limited evidence for interactions between encoding processes and consolidation effects in humans, but recent studies of consolidation in rodents have emphasized the importance of encoding "tags" for determining the impact of consolidation manipulations on memory. Here, we used functional magnetic resonance imaging in humans to test the hypothesis that the effects of post-encoding stress depend on MTL processes observed during encoding. We found that changes in stress hormone levels were associated with an increase in the contingency of memory outcomes on hippocampal and amygdala encoding responses. That is, for participants showing high cortisol reactivity, memories became more dependent on MTL activity observed during encoding, thereby shifting the distribution of recollected events toward those that had elicited relatively high activation. Surprisingly, this effect was generally larger for neutral, compared to emotionally negative, memories. The results suggest that stress does not uniformly enhance memory, but instead selectively preserves memories tagged during encoding, effectively acting as mnemonic filter. © 2016 Wiley Periodicals, Inc.

The role of eye fixation in memory enhancement under stress - An eye tracking study.

In a stressful situation, attention is shifted to potentially relevant stimuli. Recent studies from our laboratory revealed that participants stressed perform superior in a recognition task involving objects of the stressful episode. In order to characterize the role of a stress induced alteration in visual exploration, the present study investigated whether participants experiencing a laboratory social stress situation differ in their fixation from participants of a control group. Further, we aimed at shedding light on the relation of fixation behaviour with obtained memory measures. We randomly assigned 32 male and 31 female participants to a control or a stress condition consisting of the Trier Social Stress Test (TSST), a public speaking paradigm causing social evaluative threat. In an established 'friendly' control condition (f-TSST) participants talk to a friendly committee. During both conditions, the committee members used ten office items (central objects) while another ten objects were present without being used (peripheral objects). Participants wore eye tracking glasses recording their fixations. On the next day, participants performed free recall and recognition tasks involving the objects present the day before. Stressed participants showed enhanced memory for central objects, accompanied by longer fixation times and larger fixation amounts on these objects. Contrasting this, fixation towards the committee faces showed the reversed pattern; here, control participants exhibited longer fixations. Fixation indices and memory measures were, however, not correlated with each other. Psychosocial stress is associated with altered fixation behaviour. Longer fixation on objects related to the stressful situation may reflect enhanced encoding, whereas diminished face fixation suggests gaze avoidance of aversive, socially threatening stimuli. Modified visual exploration should be considered in future stress research, in particular when focussing on memory for a stressful episode.

Stress-induced cortisol hampers memory generalization.

Integrative encoding and generalization across past experiences depends largely on the hippocampus, an area known to be particularly sensitive to stress. Yet, whether stress influences the ability to generalize memories is unknown. We exposed volunteers to a stressor or a control manipulation before they completed an acquired equivalence task probing memory generalization. While stress left learning performance intact, it reduced participants' ability to generalize and this deficit was directly linked to the cortisol response to the stressor. These findings show that stress, presumably through the action of glucocorticoids, creates rather rigid memories that are difficult to transfer to novel situations.

Molar loss and powder diet leads to memory deficit and modifies the mRNA expression of brain-derived neurotrophic factor in the hippocampus of adult mice.

BACKGROUND: It is known that tooth loss is known to be a risk factor for Alzheimer's disease and soft diet feeding induces memory impairment. Recent studies have shown that brain-derived neurotrophic factor (BDNF) is associated with tooth loss or soft diet in young animal model, and that BDNF expression is decreased in patients with Alzheimer's disease. However, single or combined effect of tooth loss and/or soft diet on brain function has not fully understood. Here we examined the effect of molar loss and powder diet on memory ability and the expression of BDNF mRNA in the hippocampus of adult C57BL/6J mice. Twenty eight-weeks-old C57BL/6J mice were divided into intact molar group and extracted molar group. They were randomly divided into the I/S group (Intact upper molar teeth/Solid diet feeding), the E/S group (Extracted upper molar teeth/Solid diet feeding), the I/P group (Intact upper molar teeth/Powder diet feeding), and the E/P group (Extracted upper molar teeth/Powder diet feeding). The observation periods were 4 and 16-week. To analyze the memory ability, the step-through passive avoidance test was conducted. BDNF-related mRNA in the hippocampus was analyzed by real-time polymerase chain reaction (RT-PCR). RESULTS: At 4 weeks later, we performed memory test and isolated brains to analyze. There were no differences in memory function and BDNF mRNA level between these four groups. However, at 16 weeks later, E/S and E/P group showed memory impairment, and decreased level of BDNF mRNA. Whereas, the powder diet had no effect on memory function and BDNF mRNA level even at 16 weeks later. CONCLUSIONS: These results suggest that the effect of molar loss and powder diet on memory function and BDNF mRNA levels were different, molar loss may have a greater long-term effect on memory ability than powder diet does.

Endogenous Cortisol Exposure and Declarative Verbal Memory: A Longitudinal Study of Healthy Older Adults.

OBJECTIVE: Exposure to endogenous cortisol is associated with hippocampal degeneration and may contribute to problems with declarative memory, but effects of persistent versus phasic cortisol elevations have not been established. The present longitudinal investigation examined persistent individual differences and phasic changes in cortisol as they related to verbal memory, executive functions, and subjective cognitive function. METHODS: Older adults (n = 132, aged 60-93 years) were followed up for up to 5 years. They were assessed annually for verbal memory and every 6 months for executive functions, subjective cognitive function, and cortisol area under the curve (averaged over 3 days). RESULTS: In multilevel models, persistently but not phasically higher cortisol was associated with worse verbal memory in both learning (t(181) = 2.99, p = .003) and recall (t(280) = 3.10, p = .002). This effect withstood adjustment for stress, depression, metabolic health, and age. There was evidence for attenuated primacy in learning with higher persistent cortisol. Phasic increases in cortisol were not associated with changes in memory, and cortisol was not related to executive functions or subjective cognitive function. CONCLUSIONS: Higher secretion of cortisol may, over time, contribute to memory dysfunction in older adults.

Acute stress induces increases in salivary IL-10 levels.

The purpose of this study was to investigate the stress-reactivity of the anti-inflammatory cytokine, IL-10, in saliva and to determine how salivary IL-10 levels change in relation to those of IL-1ß, a pro-inflammatory cytokine, following stress. Healthy young adults were randomly assigned to retrieve a negative emotional memory (n = 46) or complete a modified version of the Trier Social Stress Test (n = 45). Saliva samples were taken 10 min before (baseline) and 50 min after (post-stressor) onset of a 10-min stressor, and were assayed using a high sensitivity multiplex assay for cytokines. Measurable IL-10 levels (above the minimum detectable concentration) were found in 96% of the baseline samples, and 98% of the post-stressor samples. Flow rate-adjusted salivary IL-10 levels as well as IL-1ß/IL-10 ratios showed moderate but statistically significant increases in response to stress. Measurement of salivary IL-10 and pro-/anti-inflammatory cytokine ratios may be useful, noninvasive tools, in stress research.