Stress-related Behavioral Changes Research Articles

Changes in Corticotropin-Releasing Factor Receptor Type 1, Co-Expression with Tyrosine Hydroxylase and Oxytocin Neurons, and Anxiety-Like Behaviors across the Postpartum Period in Mice

Introduction: Corticotropin-releasing factor and its primary receptor (CRFR1) are critical regulators of behavioral and neuroendocrine stress responses. CRFR1 has also been associated with stress-related behavioral changes in postpartum mice. Our previous studies indicate dynamic changes in CRFR1 levels and coupling of CRFR1 with tyrosine hydroxylase (TH) and oxytocin (OT) neurons in postpartum mice. In this study, we aimed to determine the time course of these changes during the postpartum period. Methods: Using a CRFR1-GFP reporter mouse line, we compared postpartum mice at five time points with nulliparous mice. We performed immunohistochemistry to assess changes in CRFR1 levels and changes in co-expression of TH/CRFR1-GFP and OT/CRFR1-GFP across the postpartum period. Mice were also assessed for behavioral stress responses in the open field test. Results: Relative to nulliparous mice, CRFR1 levels were elevated in the anteroventral periventricular nucleus (AVPV/PeN) but were decreased in the medial preoptic area from postpartum day 1 (P1) through P28. In the paraventricular hypothalamus (PVN), there is a transient decline in CRFR1 mid-postpartum with a nadir at P7. Co-localization of CRFR1 with TH-expressing neurons was also altered with a transient decrease found in the AVPV/PeN at P7 and P14. Co-expression of CRFR1 and OT neurons of the PVN and supraoptic nucleus was dramatically altered with virtually no co-expression found in nulliparous mice, but levels increased shortly after parturition and peaked near P21. A transient decrease in open field center time was found at P7, indicating elevated anxiety-like behavior. Conclusion: This study revealed various changes in CRFR1 across the postpartum period, which may contribute to stress-related behavior changes in postpartum mice.

Erythropoietin attenuates locomotor and cognitive impairments in male rats subjected to physical and psychological stress.

Physical and cognitive problems associated with stress are believed to result from stress-related damage to neurons involved in motor and cognitive control. In general, there are two types of stress, physical and psychological which both negatively impact neuronal function. Erythropoietin (EPO) has been shown to exert a neuroprotective effect in various models of physical brain injury; however, its actions on stress-related changes in behavior are unknown. The aim of the current study was to determine whether EPO ameliorated stress-induced locomotor and cognitive impairments, and to compare the effects of EPO on behavioral changes induced by the two different types of stressors. In this study, male Wistar rats were randomly divided into five groups and placed under physical or psychological stress for 10 consecutive days while erythropoietin was injected intraperitoneally (i.p.) every other day (500 U/kg/i.p.) 30 min before stress induction. Exploratory, anxiety-related behaviors, learning and memory were assessed by using open field, plus maze and Morris Water Maze (MWM) tests respectively. Our data showed physical and psychological stress induced dysfunction in locomotion, reduced explorative skills, heightened anxiety-like behavior and reduced memory, which could be partly reversed by EPO. We conclude that EPO reduces adverse effects of both psychological and physical stress, putatively through protection of locomotor and cognitive-controlling neurons vulnerable to the damaging effects of stress. However, future studies need to elucidate the neural mechanisms of the protective effects of EPO.

Apolipoprotein E Isoform-specific changes related to stress and trauma exposure

Post-Traumatic Stress Disorder (PTSD) is a highly prevalent mental health disorder. Due to the high level of variability in susceptibility and severity, PTSD therapies are still insufficient. In addition to environmental exposures, genetic risks play a prominent role and one such factor is apolipoprotein E. The protein (apoE) is functionally involved in cholesterol transport and metabolism and exists as 3 major isoforms in humans: E2, E3, and E4. To model the role of apolipoprotein E isoform in stress-related changes in behavior and cognition, female and male mice (3–5 months of age) expressing E2, E3, or E4 were used. Mice were either placed into control groups or exposed to chronic variable stress (CVS), which has been shown to induce PTSD-like behavioral and neuroendocrine changes. E2 mice showed a unique response to CVS compared to E3 and E4 mice that included impaired spatial learning and memory, increased adrenal gland weight, and no increase in glucocorticoid receptor protein levels (normalized to apoE levels). In addition, the cholesterol metabolite 7-ketocholesterol was elevated in the cortex after CVS in E3 and E4, but not E2 female mice. E2 confers unique changes in behavioral, cognitive, and biomarker profiles after stress exposure and identify 7-ketocholesterol as a possible novel biomarker of the traumatic stress response. We further explored the relationship between E2 and PTSD in an understudied population by genotyping 102 patients of Cambodian and Vietnamese ethnicity. E2 carriers demonstrated a higher odds ratio of having a PTSD diagnosis compared to E3/E3 carriers, supporting that the E2 genotype is associated with PTSD diagnosis after trauma exposure in this population.

Withania somnifera and Centella asiatica Extracts Ameliorate Behavioral Deficits in an In Vivo Drosophila melanogaster Model of Oxidative Stress

Due to an increase in the aging population, age-related diseases and age-related changes, such as diminished cognition and sleep disturbances, are an increasing health threat. It has been suggested that an increase in oxidative stress underlies many of these changes. Current treatments for these diseases and changes either have low efficacy or have deleterious side effects preventing long-time use. Therefore, alternative treatments that promote healthy aging and provide resilience against these health threats are needed. The herbs Withania somnifera and Centella asiatica may be two such alternatives because both have been connected with reducing oxidative stress and could therefore ameliorate age-related impairments. To test the effects of these herbs on behavioral phenotypes induced by oxidative stress, we used the Drosophila melanogaster sniffer mutant which has high levels of oxidative stress due to reduced carbonyl reductase activity. Effects on cognition and mobility were assessed using phototaxis assays and both, W. somnifera and C. asiatica water extracts improved phototaxis in sniffer mutants. In addition, W. somnifera improved nighttime sleep in male and female sniffer flies and promoted a less fragmented sleep pattern in male sniffer flies. This suggests that W. somnifera and C. asiatica can ameliorate oxidative stress-related changes in behavior and that by doing so they might promote healthy aging in humans.

Stress symptoms and Coronavirus disease 2019 (COVID-19): a comparative study between Attention Deficit Hyperactivity Disorder and typically developing children and adolescents.

Coronavirus disease 2019 (COVID-19) related confinement severely impacted people wellbeing. Many studies focused on general population, although it is reasonable to expect that patients with neurodevelopmental disorders might have been at higher risk. Children/adolescents with Attention Deficit/Hyperactivity Disorder (ADHD) might be potentially more vulnerable, due to their intolerance to forced restrictions that limit stimulating experiences, to obligation to follow instructions and to acceptation of imposed rules We aimed to compare stress-related behavioral changes of the first COVD-19 related confinement among 6-18 years old ADHD and typically developing subjects. Two parent-proxy online surveys have been employed, shared via social media. Symptoms of acute stress related to the pandemic and a question about family members/households' COVID-19 positivity have been listed in 8 yes/no items. Chi-squared tests were applied. Final sample consisted of 1078 typically developing subjects and 979 ADHD. Exaggerated startle response, difficulties in waking-up, angry mood as well as COVID-19 related fears were more prevalent among ADHD vs. typically developing subjects. typically developing subjects showed higher prevalence of research for information about COVID-19 and worries about death. In conclusion, the COVID-19 experience significantly impacted children and adolescents with ADHD to a great extent, similarly to typically developing subjects. ADHD showed more anxious-phobic responses, while typically developing subjects demonstrate more depressive attitudes. Differences in stress symptoms profiles between ADHD and T typically developing subjects warrant to develop distinct strategies of therapeutic interviews.

Activation of \u03b23-adrenoceptor increases the number of readily releasable glutamatergic vesicle via activating Ca2+/calmodulin/MLCK/myosin II pathway in the prefrontal cortex of juvenile rats

It is well known that β3-adrenoceptor (β3-AR) in many brain structures including prefrontal cortex (PFC) is involved in stress-related behavioral changes. SR58611A, a brain-penetrant β3-AR subtypes agonist, is revealed to exhibit anxiolytic- and antidepressant-like effects. Whereas activation of β3-AR exerts beneficial effects on cognitive function, the underlying cellular and molecular mechanisms have not been fully determined. In this study, whole cell patch-clamp recordings were employed to investigate the glutamatergic transmission of layer V/VI pyramidal cells in slices of the rat PFC. Our result demonstrated that SR58611A increased AMPA receptor-mediated excitatory postsynaptic currents (AMPAR-EPSCs) through activating pre-synaptic β3-AR. SR58611A enhanced the miniature EPSCs (mEPSCs) and reduced paired-pulse ratio (PPR) of AMPAR-EPSCs suggesting that SR58611A augments pre-synaptic glutamate release. SR58611A increased the number of readily releasable vesicle (N) and release probability (Pr) with no effects on the rate of recovery from vesicle depletion. Influx of Ca2+ through L-type Ca2+ channel contributed to SR58611A-mediated enhancement of glutamatergic transmission. We also found that calmodulin, myosin light chain kinase (MLCK) and myosin II were involved in SR58611A-mediated augmentation of glutamate release. Our current data suggest that SR58611A enhances glutamate release by the Ca2+/calmodulin/MLCK/myosin II pathway.

β3-adrenoceptor activation exhibits a dual effect on behaviors and glutamate receptor function in the prefrontal cortex

β-adrenoceptor (β-AR), especially the β1- and β2-AR subtypes, is known to participate in stress-related behavioral changes. Recently, SR58611A, a brain-penetrant β3-AR agonist, exhibits anxiolytic- and antidepressant-like effects. In this study, we sought to study the role of SR58611A in behavioral changes and its potential cellular and molecular mechanism in the prefrontal cortex (PFC). We found that rats with SR58611A (1 mg/kg) enhanced PFC-mediated recognition memory, whereas administration of higher dosage of SR58611A (20 mg/kg) caused hyperlocomotion, and exhibited an impairment effect on recognition memory. Electrophysiological data also indicated that SR58611A (1 mg/kg) selectively enhanced NMDA receptor-mediated excitatory postsynaptic currents (EPSC) through interacting with norepinephrine (NE) system and activating β3-AR, whereas higher dosage of SR58611A (20 mg/kg) reduced both AMPA receptor- and NMDA receptor-mediated EPSC. SR58611A-induced different effects on EPSC linked with the change of the surface expression quantity of NMDA receptor and/or AMPA receptor subunits. Synaptosomal-associated protein 25 (SNAP-25), which is a key soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein involved in incorporation of NMDA receptor to postsynaptic membrane, contributed to SR58611A (1 mg/kg)-induced enhancement of recognition memory and NMDA receptor function. Moreover, SR58611A (1 mg/kg) could rescue repeated stress-induced defect of both recognition memory and NMDA receptor function through a SNAP-25-dependent mechanism. These results provide a potential mechanism underlying the cognitive-enhancing effects of SR58611A (1 mg/kg).

690 Atopic dermatitis-induced psychological stress-related behavioral changes in NC/Nga mice model

690 Atopic dermatitis-induced psychological stress-related behavioral changes in NC/Nga mice model

Effect of ketamine on mood dysfunction and spatial cognition deficits in PTSD mouse models via HCN1–BDNF signaling

BackgroundPost-traumatic stress disorder (PTSD) is a debilitating mental disease with high morbidity and major social and economic relevance. No efficient treatment for PTSD has thus far been identified. Clinical research has shown that ketamine can rapidly alleviate symptoms in patients with chronic PTSD; however, its pharmacological mechanism has yet to be determined. MethodsThis study aimed to identify a model of single prolonged stress (SPS), which induced PTSD-like features in adult mice. Once the model was established, stress-related behavioral changes in the mouse model were evaluated after intraperitoneal injection of ketamine (10 mg/kg). Alterations in certain proteins (HCN1, BDNF, and PSD95) and synaptic ultrastructure in the prefrontal cortex (PFC) and hippocampus (HIP) were measured. ResultsThe mice under the SPS model exhibited anxiety- and depression-like behaviors and induced spatial cognitive deficits, accompanied by elevated HCN1 protein expression in the PFC and HIP, reduced brain-derived neurotrophic factor (BDNF) and PSD95 proteins, and alterations in synaptic morphology. After ketamine administration, the SPS-treated mice restored their protein levels and synaptic ultrastructure in the PFC, and their PTSD-like behaviors improved. However, learning and memory in the SPS-treated mice did not improve in the water maze test, and no significant changes in protein level and synaptic ultrastructure in the HIP were shown. LimitationsThe electrophysiological mechanism of the HCN1 ion channel after ketamine administration was not explored. ConclusionKetamine could generally improve SPS-induced mood dysfunction in mice but exerted no effect on the spatial cognitive function, which could be related to the alterations in synaptic morphology and function mediated by HCN1-related BDNF signaling in the PFC and HIP.

Enriched Environment Minimizes Anxiety/Depressive-Like Behavior in Rats Exposed to Immobilization Stress and Augments Hippocampal Neurogenesis (In Vitro).

Chronic exposure to stress disturbs the homeostasis of the brain, thus, deleteriously affecting the neurological circuits. In literature, there are investigations about the stress-related alterations in behavioral response and adult neurogenesis; however, an effective combating strategy to evade stress is still at stake. Hence, the present study is designed to investigate the effect of an enriched environment in alleviating the anxiety/depressive-like behavioral response and enhancing the adult neurogenesis in the hippocampal region of rats exposed to chronic immobilization stress. The rats were exposed to chronic immobilization stress (IS) for 4 h/day followed by the enriched environment (EE) for 2 h/day for 28days, and finally, the hippocampal region was dissected out after the behavioral analyses. IS group showed increased behavioral despair to tail suspension test, decrement in the activity for light/dark box test, and less grooming activity towards splash test. In contrast, IS + EE rats exhibited a decrease in the activity of tail suspension test and an increase in the behavioral response to light/dark box test and splash test. Thein vitro assessment of primary cultures of neurospheres from the IS group resulted in decreased levels of proliferation in the cell number and metabolic activity of both MTT assay and lactate levels. IS + EE group revealed an increase in the growth curve of neurospheres and higher metabolic activities of MTT and lactate. The IS cultures had reduced neurite length, while the neurite outgrowths were increased in IS + EE group. The IS group showed significant reduction in the protein and mRNA levels of nestin, GFAP, CD11b, MOG, and synaptophysin, whereas the IS + EE cultures exhibited significant increase in the levels of these stem cell markers. Our data highlight the positive impact of EE against stress-related behavioral changes in rats exposed to chronic immobilization stress perhaps by interfering with the differentiation of neurospheres and neurogenesis.

Kappa opioid regulation of depressive-like behavior during acute withdrawal and protracted abstinence from ethanol.

The dynorphin/kappa opioid receptor (DYN/KOR) system appears to be a key mediator of the behavioral effects of chronic exposure to alcohol. Although KOR opioid receptor antagonists have been shown to decrease stress-related behaviors in animal models during acute ethanol withdrawal, the role of the DYN/KOR system in regulating long-term behavioral changes following protracted abstinence from ethanol is not well understood. The objective of the current study was to further explore the role of the DYN/KOR system in regulating stress-related behavioral changes associated with acute withdrawal and protracted abstinence from ethanol. More specifically, the present experiments sought to examine the ability of the KOR antagonist norbinaltorphimine (nor-BNI) to reverse depressive-like behavior in the forced swim test in rats exposed to chronic ethanol. In the first experiment, rats were fed an ethanol or control liquid diet for 28–30 days, and then 24 hours after removal of the diet, were exposed to inescapable swim stress. Immediately following this procedure, rats were injected with nor-BNI (20 mg/kg) or saline and then tested 24 hours later in the forced swim test. A second experiment used a similar procedure to examine the effects of nor-BNI on behavioral changes during protracted abstinence in rats tested in the forced swim test 3 weeks after exposure to the ethanol liquid diet procedure. Ethanol-dependent rats showed increased immobility, which is thought to indicate a depressive-like state, when examined during acute withdrawal and protracted abstinence compared to controls, an effect attenuated by nor-BNI. These results suggest that the DYN/KOR system plays role in mediating both short- and long-term behavioral changes associated with depression following chronic alcohol exposure.

Chronic Vortioxetine Treatment Reduces Exaggerated Expression of Conditioned Fear Memory and Restores Active Coping Behavior in Chronically Stressed Rats.

Background:Stress is a risk factor for depression and anxiety disorders, disrupting neuronal processes leading to exaggerated fear and compromised coping behaviors. Current antidepressants are only partially effective. Vortioxetine, a novel multimodal antidepressant, is a serotonin transporter inhibitor; 5-HT3, 5-HT7, and 5-HT1D receptor antagonist; 5-HT1B partial agonist; and 5-HT1A agonist. We have shown that chronic dietary vortioxetine administration reversed stress-induced deficits in cognitive flexibility. In the present studies, we investigated the generality of vortioxetine’s effects on other stress-related behavioral changes after different types of chronic stress.Methods:In experiment 1, rats were fear-conditioned by pairing a tone with footshock, then exposed to chronic plus acute prolonged stress. In experiment 2, rats were exposed to chronic unpredictable stress. In both experiments, beginning on day 4 of chronic stress, vortioxetine was given in the diet (24 mg/kg/d). In experiment 1, effects of vortioxetine were tested on stress-induced changes in retention and extinction of cue-conditioned fear, and in experiment 2, on coping behavior on the shock probe defensive burying test after chronic stress.Results:Chronic stress exaggerated the expression of conditioned fear memory. Vortioxetine restored fear memory to control levels and rendered extinction in stressed rats comparable with that in controls. In experiment 2, chronic unpredictable stress caused a shift from active to passive coping behavior, and vortioxetine restored active coping.Conclusions:Vortioxetine reduced exaggerated expression of conditioned fear and restored adaptive coping behavior following 2 different types of chronic stress, adding to the evidence of its therapeutic potential in the management of depression and anxiety disorders.

Nitric oxide in the prelimbic medial prefrontal cortex is involved in the anxiogenic-like effect induced by acute restraint stress in rats

Neurons containing the neuronal nitric oxide synthase (nNOS) enzyme are located in brain areas related to defensive behavior, such as the ventromedial prefrontal cortex (vMPFC). Rats exposed to a live predator (a cat) present anxiety-like behavior and an increased number of nNOS-positive neurons in this brain area one-week later. Moreover, stress-related behavioral changes in rodents can be prevented by systemic or local vMPFC nNOS inhibition. In the present study we investigated if acute restraint stress (RS)-induced delayed (one-week) anxiogenic-like effect was associated with increased nNOS expression or activity in the vMPFC. Furthermore, we also tested if local pharmacological nNOS inhibition would prevent stress-induced behavioral changes. Male Wistar rats were submitted to RS for 3h and tested in the elevated plus maze (EPM) 24h or 7days later. Two hours after the EPM test, their brains were removed, processed and nNOS expression in the vMPFC was evaluated by immunohistochemistry. Another group of animals was used for measuring NO metabolites (NOx; an indirect measure of NOS activity) immediately after the EPM test, 24h after RS. Independent groups had guide cannula implanted bilaterally into the prelimbic (PL) portion of vMPFC. Five to six days after surgery, the animals were submitted to RS and 24h later received local administration of the nNOS inhibitor, N-propyl-l-arginine (NPLA; 0.04nmol). They were tested in the EPM 10min later. RS-induced anxiogenic-like effect was accompanied by increased nNOS expression in the PL (p<0.05), but not in the infralimbic (IL) vMPFC, both 24h and 7days after RS. Moreover, open-arm exploration of the EPM was negatively correlated with nNOS expression (p<0.05) and NOx levels (p<0.05) in the PL. The anxiogenic-like effect observed 24h after RS was prevented by NPLA (p<0.05). Our results suggest that RS-induced anxiogenic-like effect might depend on increased nNOS-mediated signaling in the PL MPFC.

Molecular cause and functional impact of altered synaptic lipid signaling due to a prg-1 gene SNP.

Loss of plasticity-related gene 1 (PRG-1), which regulates synaptic phospholipid signaling, leads to hyperexcitability via increased glutamate release altering excitation/inhibition (E/I) balance in cortical networks. A recently reported SNP in prg-1 (R345T/mutPRG-1) affects ~5million European and US citizens in a monoallelic variant. Our studies show that this mutation leads to a loss-of-PRG-1 function at the synapse due to its inability to control lysophosphatidic acid (LPA) levels via a cellular uptake mechanism which appears to depend on proper glycosylation altered by thisSNP. PRG-1(+/-) mice, which are animal correlates of human PRG-1(+/mut) carriers, showed an altered cortical network function and stress-related behavioral changes indicating altered resilience against psychiatric disorders. These could be reversed by modulation of phospholipid signaling via pharmacological inhibition of the LPA-synthesizing molecule autotaxin. In line, EEG recordings in a human population-based cohort revealed an E/I balance shift in monoallelic mutPRG-1 carriers and an impaired sensory gating, which is regarded as an endophenotype of stress-related mental disorders. Intervention into bioactive lipid signaling is thus a promising strategy to interfere with glutamate-dependent symptoms in psychiatric diseases.

Prise en charge de l’hypersexualité dans la maladie de Parkinson. Intérêt de la présence de l’entourage lors de l’évaluation médicale

To improve the management of hypersexuality caused by antiparkinsonian treatment and its psychopathological implications in patients with Parkinson's disease (PD). If hypersexuality is a classic form of impulse control disorder (ICD) observed in PD, its rate is certainly underestimated. We have proposed to meet patients with Parkinson's disease, referred by the neurology department of Lille University Hospital, for detection or suspicion of hypersexuality, in the presence of their spouse. The session consisted of an interview conducted by our psychiatry team. This evaluation was conducted between January 1 and August 31, 2011. Nine patients were referred to our service, 7 agreed to meet us, 6 of them with their spouse. An interview in the presence of the spouse has improved hypersexuality screening and information given to the patient and his close contacts regarding the side effects of treatment, and particularly the occurrence of hypersexuality. It also highlighted the various expressions of these behavioral changes, often minimized by patients, as spouses had great difficulty dealing with this. It helped them to improve verbal communication and, therefore, to be more informative concerning sexual behavior changes in connection with the treatment and its management. Finally, it has enabled improved support for secondary consequences of this impulse control disorder, such as guilt, jealousy or shame. Our interest has also focused on the impact of this hypersexuality on patients' families. Among the six sets partners, four had symptoms requiring specific psychiatric care: depression, suicidal intention or post-traumatic stress disorder. Hypersexuality seems underestimated in patients receiving antiparkinsonian treatment. This underestimation is probably linked to some defense mechanisms such as denial or minimization, but also to the feelings generated by these behavioral problems, such as shame or guilt. On the other hand, some patients do not experience stress related behavioral changes (even though the family may complain). Systematic partner interview could be a solution to improving this screening.

Glutamatergic mechanisms associated with stress-induced amygdala excitability and anxiety-related behavior

The neural factors underlying individual differences in susceptibility to chronic stress remain poorly understood. Preclinical studies demonstrate that mouse strains vary greatly in anxiety-related responses to chronic stress in a manner paralleled by differential stress-induced changes in glutamatergic signaling in the basolateral amygdala (BLA). Previous work has also shown that alterations in the amygdala gene expression of the GluN1 NMDA and the GluK1 kainate receptors are associated with stress-induced alterations in anxiety-like behavior in the C57BL/6J mouse strain. Using in vivo behavioral pharmacological and ex vivo physiological approaches, the aim of the current study was to further elucidate changes in glutamate neurotransmission in the BLA caused by stress and to test the functional roles of GluN1 and GluK1 in mediating stress-related changes in behavior. Results showed that stress-induced alterations in anxiety-like behavior (light/dark exploration test) were absent following bilateral infusion of the GluK1 agonist ATPA into the BLA. Intra-BLA infusion of the competitive NMDA antagonist AP5 produced a generalized behavioral disinhibition/locomotor hyperactivity, irrespective of stress. Slice electrophysiological recordings showed that ATPA augmented BLA GABAergic neurotransmission and that stress increased the amplitude of network-dependent spontaneous excitatory postsynaptic currents and amplitude of GABAergic miniature inhibitory postsynaptic currents in BLA. These findings could indicate stress-induced BLA glutamatergic neuronal network hyperexcitability and a compensatory increase in GABAergic neurotransmission, suggesting that GluK1 agonism augmented GABAergic inhibition to prevent behavioral sequelae of stress. Current data could have implications for developing novel therapeutic approaches, including GluK1 agonists, for stress-related anxiety disorders.

Stress enhances return-based behaviors in Wistar rats during spatial navigation without altering spatial performance: Improvement or deficit?

Stress is frequently reported to be deleterious to spatial learning and memory. However, there are many instances in which spatial performance is not affected by stress. This discrepancy observed across different studies, in addition to the animals' strain and gender, may be caused by the type of the task employed to assess stress-related behavioral changes. The present experiments set out to investigate the effects of repeated restraint stress (3h/21days) on spatial performance within the two wet-land (Morris water task; MWT) and dry-land (the ziggurat task; ZT) tasks for spatial learning and memory in adult male Wistar rats. All rats were tested before and after stress treatment. Stressed rats gained less weight than controls. Stress also enhanced circulating corticosterone (CORT). We did not observe a deleterious effect of stress on spatial learning and memory in either of the tasks: both groups successfully performed the wet- and dry-land tasks across all spatial testing days, indicating intact spatial cognition in control and stress rats. However, daily restraint stress for 21days significantly caused enhancement in rats' memory-dependent returns during the goal-directed investigation in the ZT. The number of returns on learning days was not affected by repeated restraint stress. Return-based spatial investigation induced by stress only on memory days in the dry-land task, not only emphasize on the task-dependent nature of stress-related alterations, it may reveal one of the silent, but arguably deleterious effects of stress on spatial memory in Wistar rats.

The 50 Hz (10 mT) sinusoidal magnetic field: effects on stress-related behavior of rats

The purpose of this study was to investigate the behavioral changes induced by 50 Hz, 10 mT flux density Sinusoidal Magnetic Field (MF). Seventy-six young adult male Wistar albino rats were used in the study. They were separated into two groups: control group (C) n=38; MF group n=38. C animals were left under the same conditions with the MF group for 21 days but with prevented or avoided exposure to MF. Anxiety and stress-related behavioral changes were investigated by elevated plus-maze and hole-board systems. Just before being tested in the maze, each animal was tested by means of the hole-board method in order to separate the directed exploration behavior and locomotion activity changes from anxiety-related behavior. In the hole-board system parameters there were no statistically significant differences between the two groups. There was a statistically significant difference between MF and C groups when the ratio of time spent on open arms to the total time spent on all arms was evaluated (0.12±0.08 and 0.34±0.18 respectively and p <0.01). Our results suggest that after 21 days, a continuous exposure to extremely low frequency of magnetic field (50 Hz, 10 mT) has no significant effect on activity and exploration activity but significantly induces stress and anxiety-related behavior in rats (Tab. 2, Fig. 9, Ref. 19).

Pituitary adenylate cyclase-activating polypeptide deficient (PACAP-/-) mice display reduced c-Fos response to forced swim stress

Event Abstract Back to Event Pituitary adenylate cyclase-activating polypeptide deficient (PACAP-/-) mice display reduced c-Fos response to forced swim stress B. Gaszner1*, V. Kormos2, D. Reglődi3, T. Kozicz4 and Z. Helyes2 1 Univ. of Pecs, Hungary 2 Pécs University, Department of Pharmacol., Hungary 3 Pécs University, Dept. of Anat., Hungary 4 Radboud University, Dept. of Cell. Animal Physiol., Netherlands PACAP-/- mice show depression-like behavior in forced swim test (FST) and hyperlocomotion in open field (OF). Examination of c-Fos expression could explore which nuclei are involved in the behavioral changes. Here we hypothesized that PACAP-/- mice vs. wildtype counterparts upon OF and FST show altered neuronal activity in stress-related areas. Our results revealed that both locomotor activity in OF and immobility in FST were greater in PACAP-/- mice in accordance with the literature. Counting of c-Fos immunoreactive neurons revealed that stress increased the activity of all examined brain areas. Stressed PACAP-/- mice showed reduced c-Fos response in the oval, anterolateral and anteromedial bed nucleus of the stria terminalis (BNST), dorsal raphe (DR) and Edinger-Westphal nuclei (EW) moreover we found stress x genotype interaction. The c-Fos expression of the periaqueductal gray matter (PAG), paraventricular nucleus (PVN) and basolateral amygdaloid nucleus (BLA) did not drop significantly in stressed PACAP-/- mice but a clear interaction between stress and genotype was observed. The ventral lateral septum (LSv) showed markedly reduced c-Fos expression in transgenic mice without interaction. c-Fos expression in the central and medial amygdala and dorsal lateral septal nucleus were not influenced by PACAP. Based on these we conclude that specific PACAP influence on the BNST, DR, EW, PAG, PVN, BLA and LSv nuclei could play a role in stress-related behavioral changes. Keywords: Behaviour and cognition, Neuroscience Conference: 13th Conference of the Hungarian Neuroscience Society (MITT), Budapest, Hungary, 20 Jan - 22 Jan, 2011. Presentation Type: Abstract Topic: Behaviour and cognition Citation: Gaszner B, Kormos V, Reglődi D, Kozicz T and Helyes Z (2011). Pituitary adenylate cyclase-activating polypeptide deficient (PACAP-/-) mice display reduced c-Fos response to forced swim stress. Front. Neurosci. Conference Abstract: 13th Conference of the Hungarian Neuroscience Society (MITT). doi: 10.3389/conf.fnins.2011.84.00128 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Mar 2011; Published Online: 23 Mar 2011. * Correspondence: Dr. B. Gaszner, Univ. of Pecs, Pécs, Hungary, balazs.b.gaszner@aok.pte.hu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes Google B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes Google Scholar B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes PubMed B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

From Classic Aspects of the Stress Response to Neuroinflammation and Sickness: Implications for Individuals and Offspring

Accumulating evidence suggests that exposure to psychological stressors leads to increased expression of pro-inflammatory cytokines and activation of inflammatory-related pathways in the central nervous system. Several logical predictions arise from these findings: (1) stressor exposure should produce changes in behavior that are reminiscent of acute illness; (2) administration of antiinflammatory agents should ameliorate some behavioral consequences of stressor exposure; and (3) there should be convergence between anatomical and neurochemical pathways activated by stressor exposure and those involved in mitigating sickness behaviors. Importantly, these predictions have been tested in our laboratory across multiple stressor paradigms (footshock, maternal separation, and during acute alcohol withdrawal) using two species (rats and guinea pigs), suggesting that sickness may represent a more general motivational state that can be elicited by a diverse range of psychological challenges. Implications of these findings for understanding stress-related changes in behavior, mood and neuroinflammatory processes will be discussed with special reference to implications for the individual and reproductive fitness.