Neuroendocrine response to a psychosocial stress test is not related to schizotypy but cortisol elevation predicts inflexibility of semantic memory retrieval.

An altered stress response can contribute to the transition from preclinical psychotic symptoms to the clinical manifestation of schizophrenia and other psychotic disorders. The present study was aimed at testing the hypotheses that (i) the autonomic and neuroendocrine responses under psychosocial stress are dysregulated in individuals with high psychosis proneness (schizotypy); (ii) the magnitude of post-stress autonomic activation and cortisol release predicts alterations in semantic memory retrieval. The study was performed in 73 healthy individuals of both sexes with either high or low schizotypal traits preselected out of 609 individuals using the Schizotypal Personality Questionnaire. A psychosocial stress procedure based on public speech was used as a stress model. We found that individuals with high schizotypy engaged in less adaptive emotional stress-coping strategies than low schizotypy individuals. Yet, the neuroendocrine, immune, and sympathetic activation in response to the stress test was not different between the groups. Irrespective of the exposure to the stressor, individuals with high schizotypy were less fluent when retrieving associations from semantic memory. In addition, we demonstrated that acute psychosocial stress reduced the flexibility of semantic memory retrieval. The post-stress mental inflexibility was reliably predicted by the concomitant elevation of cortisol concentrations in saliva. The present study thus brings novel evidence indicating that the acute psychosocial challenge impairs retrieval flexibility in the semantic domain, which may be due to neuroendocrine activation.

Chronic treatment with enhancer drugs modifies the gene expression of selected parameters related to brain plasticity in rats under stress conditions.

Selegiline, also known as L-deprenyl, and (2R)-1-(1-benzofuran-2-yl)-N-propylpentane-2-amine (BPAP) were found to induce enhancement of monoamine neurotransmission in low and very low doses. In addition, these enhancers may modify glutamatergic neurotransmission. The aim of the present study was to test the hypothesis that under stress conditions, chronic treatment with enhancer drugs has a positive impact on the glutamatergic system and other parameters related to brain plasticity, stress-related systems, and anxiety behavior. We exposed male Wistar rats to a chronic mild stress procedure combined with chronic treatment with two synthetic enhancer drugs. The gene expression of GluR1, an AMPA receptor subunit was reduced by repeated treatment with deprenyl in the hippocampus and with both BPAP and deprenyl in the prefrontal cortex. A significant reduction of NMDA receptor subunit GluN2B expression was observed in the hippocampus but not in the prefrontal cortex. Deprenyl treatment led to an enhancement of hippocampal BDNFmRNA concentrations in stress-exposed rats. Treatment with enhancer drugs failed to induce significant changes in stress hormone concentrations or anxiety behavior. In conclusion, the present study in chronically stressed rats showed that concomitant treatment with enhancer drugs did not provoke substantial neuroendocrine changes, but modified gene expression of selected parameters associated with brain plasticity. Observed changes may indicate a positive influence of enhancer drugs on brain plasticity, which is important for preventing negative consequences of chronic stress and enhancement of stress resilience. It may be suggested that the changes in glutamate receptor subunits induced by enhancer drugs are brain region-specific and not dose-related.

Testosterone but not cortisol concentrations in hair correlate between mothers and their prepubertal children under real-life stress conditions.

The aim of the present study is to test the hypothesis that there is an association between the neuroendocrine state, reflected by testosterone and cortisol concentrations in hair, of the mother and her child under difficult real-life stress conditions (COVID-19 pandemic). The research sample consisted of 45 healthy mothers and their prepubertal children (7 - 11 years) of both sexes. The hair samples of mother-child dyads were collected twice to obtain cumulative stress hormone concentrations from April till the end of June and July till the end of September 2020. Thus, 90 mother-child pairs were analyzed. The results showed that both cortisol and testosterone concentrations were significantly higher in the hair of mothers compared to those in their children. The results of cortisol concentrations in hair do not support the hypothesis stated above. In line with our hypothesis are the results of hair testosterone measurements showing a positive correlation between testosterone concentrations in mothers and their children. With respect to the known relationship of testosterone with aggressive behavior, an important finding is that above-mentioned correlation was particularly strong in women with intense subjective feelings of anger in the investigated three months period. Women with strongly prevalent subjective feelings of sadness failed to show a significant correlation between hair cortisol concentrations in mothers and their children, in spite of the known relationship of cortisol to depressive mood. It may be suggested that chronic testosterone secretion reflects the association between the neuroendocrine function of the mother and her child under real-life stress conditions.

Salivary testosterone, testosterone/cortisol ratio and non-verbal behavior in stress.

The relationship between hormone release and non-verbal communication under stress conditions is still not sufficiently explored. The aim of the present study was to test the hypothesis that salivary testosterone concentrations and testosterone/cortisol (T/C) ratios correlate positively with assertive behavior representing a non-aggressive form of dominance during an acute stress situation. As a stress model, a socially evaluated cold pressor test was investigated in healthy men. The non-verbal behavior was analyzed according to the ethological coding system for interviews described by Troisi (1999). Salivary testosterone concentrations did not change throughout the stress test. The T/C ratios decreased significantly over time only in subjects showing high stress perception. The duration of affiliative and the frequency of flight behavior was higher in subjects with high stress perception compared to those with low stress perception. A significant positive correlation between the duration of prosocial behavior and values of T/C ratios was found in the whole sample. The area under the curve values of testosterone positively correlated with the duration of assertive behavior in the group with high stress perception and negatively in the other group. Our findings allow suggesting that the changes in non-verbal behavior during acute psychosocial stress situations may be more pronounced in subjects showing high stress perception. Obtained results motivate further research on a better understanding of the consequences of the lack of sense of full facial expressions, such as wearing face masks, on the balance between hormones and non-verbal behavior under stress conditions.

Delta-Opioid Receptors Play a Role in the Control of Selected Parameters Related to Stress and Brain Plasticity Under Non-stress and/or Stress Conditions.

There is some evidence that delta-opioid receptors may be involved in the brain processes related to neuroprotection. The aim of the present studies was to test the hypothesis that endogenous opioid peptides acting via delta-opioid receptors can protect against stress-induced changes in factors related to brain plasticity and stress hormone release. Forty male adult Wistar rats were used. Half of the animals were exposed to sustained partial restraint stress (hypokinesis) lasting 48 h. Rats were treated with vehicle (isotonic saline) or the delta-opioid receptor antagonist naltrindole (3 mg/kg/ml, s.c.) six times a day. The stressfulness of the model was confirmed by increased plasma concentrations of corticosterone and prolactin, the increase in anxiety behavior in the open field test, as well as the reduction of BrdU incorporation into newly formed DNA in the hippocampus. Treatment with naltrindole potentiated the stress-induced rise in aldosterone concentrations. The blockade of delta-opioid receptors resulted in a decrease in hippocampal BDNF gene expression independently of control or stress conditions. Treatment with naltrindole enhanced plasma concentrations of copeptin, a stable precursor of vasopressin. In conclusion, these results suggest that endogenous opioid peptides might play an inhibitory role in aldosterone release under stress conditions and in the control of vasopressin release independently of stress exposure. Endogenous opioids might stimulate hippocampal gene expression of the important neurotrophic factor BDNF via delta-opioid receptors.

Cumulative cortisol concentrations in hair of patients with atopy are lower than in healthy subjects and are not related to their perceived stress experience.

Patients with atopy were found to exhibit blunted cortisol responses to acute stress stimuli. The aim of this study was to test the hypothesis that cumulative cortisol concentrations in the hair of patients with atopy are lower than in healthy subjects when related to their perceived stress experience. The sample consisted of 31 participants. The most proximal 3 cm of hair (as close to the scalp as possible), reflecting the cumulative cortisol secretion during the previous 3 months, was used for the analysis. Only in 20 subjects (9 patients with atopy and 11 healthy controls), there was a sufficient amount of hair for precise analysis using a new methodology. The results showed lower hair cortisol concentrations in patients with atopy compared to those in controls. The perceived stress scores in patients with atopy and healthy controls were not statistically different. The cortisol concentration/perceived stress score ratios were lower in patients with atopy compared to those in controls. No statistically significant correlation between hair cortisol and long-term experienced stress assessed via perceived stress scale was observed. In conclusion, the cumulative cortisol secretion in the hair of atopic patients is lower than would be expected according to their subjective scores of perceived stress. Most importantly, the previously lower stress hormone increase found in acute stress situations and in children now was confirmed in adult patients with chronic stress load.

Voluntary exercise may activate components of pro-survival risk pathway in the rat heart and potentially modify cell proliferation in the myocardium.

Although physical exercise is known to reduce size of infarction, incidence of ventricular arrhythmias, and to improve heart function, molecular mechanisms of this protection are not fully elucidated. We explored the hypothesis that voluntary running, similar to adaptive interventions, such as ischemic or remote preconditioning, may activate components of pro-survival (RISK) pathway and potentially modify cell proliferation. Sprague-Dawley adult male rats freely exercised for 23 days in cages equipped with running wheels, while sedentary controls were housed in standard cages. After 23 days, left ventricular (LV) myocardial tissue samples were collected for the detection of expression and activation of RISK proteins (WB). The day before, a marker of cell proliferation 5-bromo-2'-deoxyuridine (BrdU) was given to all animals to detect its incorporation into DNA of the LV cells (ELISA). Running increased phosphorylation (activation) of Akt, as well as the levels of PKC? and phospho-ERK1/2, whereas BrdU incorporation into DNA was unchanged. In contrast, exercise promoted pro-apoptotic signaling - enhanced Bax/Bcl-2 ratio and activation of GSK-3ß kinase. Results suggest that in the rat myocardium adapted to physical load, natural cardioprotective processes associated with physiological hypertrophy are stimulated, while cell proliferation is not modified. Up-regulation of pro-apoptotic markers indicates potential induction of cell death mechanisms that might lead to maladaptation in the long-term.

Behavioral alterations induced by post-weaning isolation rearing of rats are accompanied by reduced VGF/BDNF/TrkB signaling in the hippocampus.

Post-weaning social isolation has been shown to be a relevant animal model for studying the mechanisms underlying psychopathological states induced by early-life stressful experiences. Besides extensively studied brain-derived neurotrophic factor (BDNF) and tyrosine receptor kinase B (TrkB) receptor, increasing attention is being given to a neuropeptide precursor VGF (non-acronymic). Several lines of evidence indicate an interplay between the neurotrophins and nitric oxide signaling. This study investigated the long-term consequences of post-weaning social isolation on behavior, VGF/BDNF/TrkB pathway and two isoforms of nitric oxide synthase (NOS) in the hippocampus and examined whether these effects were sex-specific. Male and female Sprague-Dawley rats were reared either in social isolation or social groups from postnatal day 21 for 9 weeks (n = 12-15/group and sex). Post-weaning social isolation induced impairments in sensorimotor gating and increased anxiety-like behavior in rats of both sexes. These behavioral alterations were accompanied by attenuated gene expression of VGF and TrkB receptor in the hippocampus. Isolation-induced reduction in VGF gene expression was more evident in male isolates. Similar changes were found in neuronal NOS (nNOS) gene expression with reduced mRNA levels in male isolates. Gene expression of BDNF and inducible NOS was not influenced by isolation rearing or sex. In addition, sex-specific patterns of VGF and nNOS gene expression in the hippocampus with higher mRNA levels in males than in females were revealed. The present study demonstrates a relationship between nNOS, VGF, BDNF, and TrkB confirming a link between nitric oxide and neurotrophins signaling pathways. Our findings indicate that long-term post-weaning social isolation alters signaling via VGF/BDNF/TrkB and nNOS that could interfere with neurodevelopmental processes which may contribute to pathological behavioral symptoms in adulthood. Future studies are needed to support this suggestion since the direct mechanistic link has not been approached in this study.

Patients with atopy exhibit reduced cortisol awakening response but not cortisol concentrations during the rest of the day.

It has been documented that cortisol release in response to acute stressors is reduced in patients with atopic dermatitis, allergic rhinitis, and other atopic diseases compared to that in healthy subjects. We aimed to test the hypothesis that atopic patients exert reduced salivary cortisol awakening response (CAR) in comparison with healthy subjects. The hypothesis was tested on a stressful and a relax day selected subjectively. Moreover, we evaluated the impact of trait anxiety. The sample consisted of 60 subjects, out of which 28 were patients with atopy and 32 healthy volunteers of both sexes. Saliva samples were collected in the morning to evaluate CAR as well as in the early afternoon and evening to look at cortisol concentrations during the rest of the day. The results showed reduced CAR in atopic patients compared to that in healthy subjects. This effect was modulated by sex with a significant difference observed in males. While CAR was reduced, atopic patients had unchanged cortisol concentrations throughout the day. The evening cortisol was even higher in atopic patients. If the subjects were stratified according to the trait anxiety, no significant differences in CAR between high and low anxiety were observed. No differences in cortisol variables including CAR were observed between the stressful and relax day. In conclusion, this study presents evidence on reduced CAR suggesting an insufficient HPA axis reactivity in atopy. Furthermore, the data in atopic patients demonstrate that reduced HPA axis reactivity does not necessarily mean lower cortisol concentrations throughout the day. This might be of relevance to immune system function and the course of the disease.

Aldosterone and aldosterone/cortisol ratio is higher in serum of long-term compared to first episode schizophrenia patients: A pilot study.

We have previously shown that patients with severe depressive episode exhibit higher aldosterone concentrations compared to those with moderate depressive episode. The present study was undertaken to test the hypothesis that circulating concentration of aldosterone reflect the clinical state in patients with schizophrenia. The sample consisted of 36 hospitalized patients (25 men, 11 women) with the first episode or long-term course of schizophrenia. The severity of psychopathology was evaluated using the Positive and Negative Syndrome Scale (PANSS). Samples for measurement of serum aldosterone were obtained immediately after awakening. The results showed that serum aldosterone concentrations were lower in patients with the first episode compared to those in patients with long-term course of schizophrenia. Importantly, lower aldosterone concentrations observed in patients with the first episode were associated with more severe clinical symptoms as indicated by all subscales of PANSS. Serum cortisol concentrations did not differ between the groups, while the aldosterone/cortisol ratio showed similar pattern as aldosterone concentrations. The present pilot study suggests that circulating aldosterone in patients with schizophrenia may reflect the severity of clinical symptoms but in an opposite direction than in patients with major depressive disorder.

Effects of vortioxetine on biomarkers associated with glutamatergic activity in an SSRI insensitive model of depression in female rats.

The aim of this study was to investigate the antidepressant activity of vortioxetine in a tryptophan (TRP) depletion female rat model of depression and compare it to that of paroxetine using doses that fully occupy the serotonin transporter (SERT). We evaluated the effects of vortioxetine on potential biomarkers associated with TRP depletion including serum aldosterone, corticosterone and IL-6 levels together with indirect indicators of glutamate neurotransmission. Female Sprague-Dawley rats were randomized to control, low TRP, low TRP/paroxetine or low TRP/vortioxetine groups. Vortioxetine and paroxetine were administered via diet (10mg/kg/day) and drinking water (10mg/kg/day) respectively for 14days. Vortioxetine but not paroxetine reversed TRP depletion-induced depressive-like behavior. Vortioxetine reduced TRP depletion-induced increases of serum corticosterone, aldosterone, IL-6 and N-methyl-d-aspartate and α7-nicotinic acetylcholine receptor expression in the amygdala and hippocampus, respectively. Paroxetine demonstrated little effect except a reduction of aldosterone. Vortioxetine but not paroxetine reversed TRP depletion-induced reductions of serum and brain kynurenic acid. In conclusion, vortioxetine, but not paroxetine, enabled reversals of TRP depletion-induced changes of depression-like behavior and markers of glutamatergic activity. These observations support the hypothesis that vortioxetine's antidepressant activity may involve mechanisms beyond SERT inhibition.

Reprint of: Contrasting effects of vortioxetine and paroxetine on pineal gland biochemistry in a tryptophan-depletion model of depression in female rats.

We studied the effects of the multi-modal antidepressant, vortioxetine and the SSRI, paroxetine on pineal melatonin and monoamine synthesis in a sub-chronic tryptophan (TRP) depletion model of depression based on a low TRP diet. Female Sprague-Dawley rats were randomised to groups a) control, b) low TRP diet, c) low TRP diet+paroxetine and d) low TRP diet+vortioxetine. Vortioxetine was administered via the diet (0.76mg/kg of food weight) and paroxetine via drinking water (10mg/kg/day) for 14days. Both drugs resulted in SERT occupancies >90%. Vortioxetine significantly reversed TRP depletion-induced reductions of pineal melatonin and serotonin (5-HT) and significantly increased pineal noradrenaline NA. Paroxetine did none of these things. Other studies suggest pineal melatonin synthesis may involve N-methyl-d-aspartate (NMDA) receptors and glutamatergic modulation. Here observed changes may be mediated via vortioxetine's strong 5-HT reuptake blocking action together with possible additional effects on glutamate neurotransmission in the pineal via NMDA receptor-modulation and possibly with added impetus from increased NA output.

Contrasting effects of vortioxetine and paroxetine on pineal gland biochemistry in a tryptophan-depletion model of depression in female rats.

We studied the effects of the multi-modal antidepressant, vortioxetine and the SSRI, paroxetine on pineal melatonin and monoamine synthesis in a sub-chronic tryptophan (TRP) depletion model of depression based on a low TRP diet. Female Sprague-Dawley rats were randomised to groups a) control, b) low TRP diet, c) low TRP diet+paroxetine and d) low TRP diet+vortioxetine. Vortioxetine was administered via the diet (0.76mg/kg of food weight) and paroxetine via drinking water (10mg/kg/day) for 14days. Both drugs resulted in SERT occupancies >90%. Vortioxetine significantly reversed TRP depletion-induced reductions of pineal melatonin and serotonin (5-HT) and significantly increased pineal noradrenaline NA. Paroxetine did none of these things. Other studies suggest pineal melatonin synthesis may involve N-methyl-d-aspartate (NMDA) receptors and glutamatergic modulation. Here observed changes may be mediated via vortioxetine's strong 5-HT reuptake blocking action together with possible additional effects on glutamate neurotransmission in the pineal via NMDA receptor-modulation and possibly with added impetus from increased NA output.

Aldosterone concentrations in saliva reflect the duration and severity of depressive episode in a sex dependent manner.

Evidence is accumulating that aldosterone may exert central actions and influence mental functions. The aim of the present study was to test the hypothesis that major depressive disorder affects the diurnal variation of salivary aldosterone and that aldosterone concentrations reflect the duration and severity of the depressive episode in a sex dependent manner. The sample consisted of 60 patients (37 postmenopausal women, 23 men) with major depressive disorder. Patients were examined two times, in acute depressive episode (admission to the hospital) and after reaching clinical remission (discharge). The samples of saliva were taken by the patients themselves twice a day (8.00-9.00 h in the morning and in the evening). Aldosterone concentrations were significantly higher in women compared to men and were significantly higher at the time of admission to the hospital compared to those at the discharge. Morning but not evening salivary aldosterone concentrations reflected the length of the depressive episode in women as well as the severity of the disorder in both sexes. Moreover, the patients with depression failed to exert known daily rhythmicity of aldosterone release. The present study brings several pieces of evidence suggesting the association of aldosterone with the pathophysiology of depression. Salivary aldosterone concentrations appear to reflect the outcome, the duration and the severity of the depressive episode in a sex dependent manner.

Individual prolactin reactivity modulates response of nucleus accumbens to erotic stimuli during acute cannabis intoxication: an fMRI pilot study.

RATIONALE: Self-report studies indicate that cannabis could increase sexual desire in some users. We hypothesized that intoxication increases activation of brain areas responsive to visual erotica, which could be useful in the treatment of hypoactive sexual desire disorder, a condition marked by a lack of sexual desire. OBJECTIVES: The aim of this study is to assess the aphrodisiacal properties of cannabis. METHODS: We conducted an open-randomized study with 21 heterosexual casual cannabis users. A 3T MRI was used to measure brain activation in response to erotic pictures. Blood samples were collected to determine the serum levels of cannabinoids, cortisol and prolactin. Participants were grouped according to whether they had ever experienced any aphrodisiacal effects during intoxication (Group A) or not (Group non-A). RESULTS: Intoxication was found to significantly increase activation in the right nucleus accumbens in the Group A while significantly decreasing activation in the Group non-A. There was also a significant interaction between the group and intoxication, with elevated prolactin in the Group non-A during intoxication. No intoxication-related differences in subjective picture evaluations were found. CONCLUSION: Cannabis intoxication increases activation of the right nucleus accumbens to erotic stimuli. This effect is limited to users whose prolactin is not elevated in response to intoxication. This effect may be useful in the treatment of low sexual desire.

Blunted cortisol response to psychosocial stress in atopic patients is associated with decrease in salivary alpha-amylase and aldosterone: Focus on sex and menstrual cycle phase.

A decreased responsiveness of the hypothalamic-pituitary-adrenocortical axis to stress stimuli in patients with atopy is well documented. The aim of this study was to investigate personality traits, salivary alpha-amylase activity and the aldosterone response to psychosocial stress procedure based on public speech in atopic patients with respect to sex and the menstrual cycle (MC) phase. The study was performed in 106 subjects of both sexes, 53 atopic patients suffering from allergic rhinitis, allergic asthma or atopic dermatitis and 53 age-, sex-, the MC phase- and BMI- matched healthy controls. Substantially attenuated activity of alpha-amylase and reduced secretion of aldosterone during the psychosocial stress were observed in the whole sample of patients with atopy. Higher activity of alpha-amylase observed in the follicular compared to the luteal phase in healthy women was not present in atopic patients. In both males and females, atopy was associated with blunted cortisol response but no changes in the heart rate. Psychological characterization revealed a significantly higher trait anxiety and higher preference for avoidance-oriented coping strategy in female but not male atopic patients. These findings provide evidence that patients with atopy exhibit insufficient alpha-amylase and aldosterone responsiveness to psychosocial stress, thus suggesting decreased sympathetic activity. Potential disturbances in sex hormone status during the MC in female patients with atopy have to be considered in future research. Changes in personality traits were demonstrated in female atopic patients, but not in male patients.

Increased gene expression of selected vesicular and glial glutamate transporters in the frontal cortex in rats exposed to voluntary wheel running.

Though positive effects of exercise on mood and well being are well recognised, the central regulatory mechanisms are still not fully understood. The present study was aimed to testing the hypothesis that voluntary wheel running activates the gene expression of glutamate transporters in the brain cortex of rats. The animals were assigned to the control and voluntary wheel running groups. Voluntary wheel running rats had free access to a stainless steel activity wheel for 3 weeks. The daily running distance gradually increased to 6.21 ± 1.05 km by day 21. Vesicular glutamate transporter 3 (VGLUT3) mRNA levels in the frontal cortex were significantly elevated in the group of running animals compared to the values in sedentary controls, while the expression of other vesicular transporters were unchanged. The concentrations of mRNA coding for glial glutamate transporter 1 (GLT-1), but not glutamate aspartate transporter (GLAST) were increased by running. Voluntary wheel running resulted in an elevation of plasma corticosterone and increased expression of brain derived neurotrophic factor (BDNF) in the frontal cortex. In conclusion, chronic voluntary wheel running results in increased gene expression of VGLUT3 and GLT-1 in the brain cortex without changes in other glutamate transporter subtypes.

Metabolic effects of subchronic peripheral oxytocin administration in lean and obese zucker rats.

Increasing evidence indicates a role of oxytocin in controlling energy metabolism. The aim of his study was to investigate oxytocin effects on obese phenotype in leptin-resistant Zucker fatty rats, focusing on glucose and lipid metabolism. Zucker fatty rats and their lean controls were treated with oxytocin (3.6 µg/100g body weight/day) by osmotic minipumps implanted subcutaneously for 2 weeks. Two-hours intraperitoneal glucose tolerance test was performed in fasting rats. Oxytocin decreased food intake in both phenotypes while body weight gain reduced only in obese animals. In obese rats oxytocin impaired hepatic insulin extraction and enhanced liver triglyceride accumulation. Moreover, in the skeletal muscle of lean rats oxytocin treatment downregulated insulin signal transduction by decreasing of insulin receptor substrate 1 protein level and stimulating of its serine phosphorylation. Concurrently, the gene expression of insulin receptor substrate 1 in the skeletal muscle and adipose tissue was downregulated by oxytocin. In obese rats, oxytocin reduced adipocyte size and normalised mRNA levels of both fatty acid binding protein 4 and fatty acid synthase but attenuated gene expression of glucose transporter 4. The present study in Zucker fatty rats demonstrated ambivalent effects of oxytocin treatment with predominantly negative impact on skeletal muscle insulin pathway in lean animals.

Psychosocial stress based on public speech in humans: is there a real life/laboratory setting cross-adaptation?

Repeated or chronic exposure to stressors is associated with changes in neuroendocrine responses depending on the type, intensity, number and frequency of stress exposure as well as previous stress experience. The aim of the study was to test the hypothesis that salivary cortisol and cardiovascular responses to real-life psychosocial stressors related to public performance can cross-adapt with responses to psychosocial stress induced by public speech under laboratory setting. The sample consisted of 22 healthy male volunteers, which were either actors, more precisely students of dramatic arts or non-actors, students of other fields. The stress task consisted of 15 min anticipatory preparation phase and 15 min of public speech on an emotionally charged topic. The actors, who were accustomed to public speaking, responded with a rise in salivary cortisol as well as blood pressure to laboratory public speech. The values of salivary cortisol, systolic blood pressure and state anxiety were lower in actors compared to non-actors. Unlike non-actors, subjects with experience in public speaking did not show stress-induced rise in the heart rate. Evaluation of personality traits revealed that actors scored significantly higher in extraversion than the subjects in the non-actor group. In conclusion, neuroendocrine responses to real-life stressors in actors can partially cross-adapt with responses to psychosocial stress under laboratory setting. The most evident adaptation was at the level of heart rate responses. The public speech tasks may be of help in evaluation of the ability to cope with stress in real life in artists by simple laboratory testing.

Inhibition of fatty-acid amide hydrolyse (FAAH) exerts cognitive improvements in male but not female rats.

OBJECTIVES: The endocannabinoid system is implicated in the regulation of various brain functions including cognition, memory, and behavior. It has been shown that inhibition of the endocannabinoid-degrading enzyme fatty acid amid hydrolase (FAAH) enhances the memory and learning in males. Given the fact that sexual dimorphism exists in the different components of the endocannabinoid system, the aim of this study was to test the hypothesis that cognition enhancing effect of the acute inhibition of FAAH by URB597 is gender dependent. METHODS: In the study, 32 adult male and female Sprague-Dawley rats were used. They were treated with a single intraperitoneal injection of FAAH inhibitor URB597 (0.3 mg/kg) or vehicle 40 min before behavioral testing. The novel object recognition test was used as a working memory task to assess cognitive performance. RESULTS: Neither the treatment nor the gender significantly affected the velocity, the total distance travelled and the time spent exploring the familiar object. The recognition of the object was influenced by both URB597 and gender. Male rats treated with URB597 displayed significantly increased novel object exploration compared to males treated with vehicle as well as to female rats treated with URB597. Single administration of URB597 significantly enhanced the recognition index in male, but not female rats. CONCLUSIONS: The results demonstrate that the positive effects of FAAH inhibition on the cognition are gender dependent. It is likely that male rats are more vulnerable to the modulation of the endocannabinoid system than female rats.