Forms Of Psychological Stress Research Articles

Sex-Specific Alterations in Spatial Memory and Hippocampal AKT-mTOR Signaling in Adult Mice Pre-exposed to Ketamine and/or Psychological Stress During Adolescence

BackgroundKetamine (KET) is administered to manage major depression in adolescent patients. However, the long-term effects of juvenile KET exposure on memory-related tasks have not been thoroughly assessed. We examined whether exposure to KET, psychological stress, or both results in long-lasting alterations in spatial memory in C57BL/6 mice. Furthermore, we evaluated how KET and/or psychological stress history influenced hippocampal protein kinase B–mechanistic target of rapamycin (AKT-mTOR)–related signaling. MethodsOn postnatal day 35, male and female mice underwent vicarious defeat stress (VDS), a form of psychological stress that reduces sociability in both sexes, with or without KET exposure (20 mg/kg/day, postnatal days 35–44). In adulthood (postnatal day 70), mice were assessed for spatial memory performance on a water maze task or euthanized for hippocampal tissue collection. ResultsJuvenile pre-exposure to KET or VDS individually increased the latency (seconds) to locate the escape platform in adult male, but not female, mice. However, juvenile history of concomitant KET and VDS prevented memory impairment. Furthermore, individual KET or VDS pre-exposure, unlike their combined history, decreased hippocampal AKT-mTOR signaling in adult male mice. Conversely, KET pre-exposure alone increased AKT-mTOR in the hippocampus of adult female mice. Lastly, rapamycin-induced decreases of mTOR in naïve adult female mice induced spatial memory retrieval deficits, mimicking adult male mice with a history of exposure to VDS or KET. ConclusionsOur preclinical model shows how KET treatment for the management of adolescent psychological stress–induced sequelae does not impair spatial memory later in life. However, juvenile recreational KET misuse, like psychological stress history, results in long-term spatial memory deficits and hippocampal AKT-mTOR signaling changes in a sex-specific manner.

Resilience of Teachers in Special Education Schools in Guizhou Province, China through Administration: Ecological Systems Theory Analysis

Background and Aims: This paper aim to investigate that teachers in special education schools have poor teacher resilience, mainly in the form of psychological stress that leads to mental health problems and consequent poor teaching effectiveness. Methods: Through the quantitative approach, this paper investigates the phenomenon. Results: The results suggest that special education schools should develop a comprehensive support system for in-service teachers in their administration based on the interaction of the systems within, between, beyond, and the cross system. Conclusion: It is hoped that through the adaptation of classroom teaching methods and materials to the realities of special education, collaboration between general education teachers and special education teachers, and the establishment of a school culture that respects individual differences, the aim is to enhance the teacher resilience of teachers in special education schools.

Psychological stress is associated with arterial inflammation in people living with treated HIV infection

Stress and depression are increasingly recognized as cerebrovascular risk factors, including among high stress populations such as people living with HIV infection (PLWH). Stress may contribute to stroke risk through activation of neural inflammatory pathways. In this cross-sectional study, we examined the relationships between stress, systemic and arterial inflammation, and metabolic activity in stress-related brain regions on 18F-fluorodeoxyglucose (FDG)-PET in PLWH. Participants were recruited from a parent trial evaluating the impact of alirocumab on radiologic markers of cardiovascular risk in people with treated HIV infection. We administered a stress battery to assess different forms of psychological stress, specifying the Perceived Stress Scale as the primary stress measure, and quantified plasma markers of inflammation and immune activation. Participants underwent FDG-PET of the brain, neck, and chest. Age- and sex-matched control participants without HIV infection were selected for brain FDG-PET comparisons. Among PLWH, we used nonparametric pairwise correlations, partial correlations, and linear regression to investigate the association between stress and 1) systemic inflammation; 2) atherosclerotic inflammation on FDG-PET; and metabolic activity in 3) brain regions in which glucose metabolism differed significantly by HIV serostatus; and 4) in a priori defined stress-responsive regions of interest (ROI) and stress-related neural network activity (i.e., ratio of amygdala to ventromedial prefrontal cortex or temporal lobe activity). We studied 37 PLWH (mean age 60 years, 97% men) and 29 control participants without HIV (mean age 62 years, 97% men). Among PLWH, stress was significantly correlated with systemic inflammation (r = 0.33, p = 0.041) and arterial inflammation in the carotid (r = 0.41, p = 0.023) independent of age, race/ethnicity, traditional vascular risk factors and health-related behaviors. In voxel-wise analyses, metabolic activity in a cluster corresponding to the anterior medial temporal lobes, including the bilateral amygdalae, was significantly lower in PLWH compared with controls. However, we did not find a significant positive relationship between stress and this cluster of decreased metabolic activity in PLWH, a priori defined stress-responsive ROI, or stress-related neural network activity. In conclusion, psychological stress was associated with systemic and carotid arterial inflammation in this group of PLWH with treated infection. These data provide preliminary evidence for a link between psychological stress, inflammation, and atherosclerosis as potential drivers of excess cerebrovascular risk among PLWH.

Risk Perception, Behavior Change and Perceived Impact due to COVID-19 Pandemic among General Population in Tamil Nadu, India: A Cross-Sectional Study

Background: Coronavirus disease 2019 (COVID-19) has affected countries all over the world. Assessment of risk perception and scaling up appropriate behavioral practices are of utmost importance for its prevention and control. The objectives of this study were identifying risk perception, behavioral changes and perceived impact as a result of COVID-19 and its associated factors among general population.
 Methods: A cross-sectional study was done during the first wave of COVID-19 among general population in Tamil Nadu, India. A semi-structured questionnaire was prepared in Google forms and circulated using whatsapp during April and June 2020. The sample size was calculated at 384. Data were analyzed using SPSS software version 21.0. Association between the variables was analyzed using Chi-square test. P-value <0.05 was considered significant. 
 Results: Mean age was 38.4 ±13.8, and 52.1% of the participants were females. Almost 2/3rdhad perceived risk of catching COVID-19, which was more among respondents aged 20-39 and residing in urban area. Among the behavior change measures, wearing mask in public places was practiced by 95%, followed by hand washing (90.4%) and social distancing (80%). More than 50% had some form of psychological stress that included inability to perform their daily routines, anxiously browsing media for information about COVID-19, not going to work .etc.
 Conclusion: General public staying in rural areas have not completed secondary school education, and the elderly have to be targeted to provide appropriate information about COVID-19 and its preventive measures.

Mental health and work-related factors in healthcare workers in a pandemic – meta-analysis

ABSTRACT Due to the SARS-CoV-2 pandemic, healthcare workers worldwide faced major challenges in the form of psychological stress. The aim of this systematic literature review and meta-analysis is to identify mental health consequences and associated work-related factors in healthcare workers during a pandemic and to quantify the influence of associated work-related factors on mental health consequences. A systematic literature search according to PRISMA was conducted on 5 August 2021 using the databases PubMed Central and APA PsychInfo. The included studies investigated the mental health consequences and associated work-related factors in healthcare workers in a pandemic. In addition, we performed a risk of bias analysis to assess the study quality of the included studies using the JBI checklists. Random-effect models and pooled effect estimators were used for the meta-analysis. The Chi2 and I2 statistics were used to identify the statistical heterogeneity. Additional sensitivity analysis was performed. From a total of 3,910 publications, 43 studies met the inclusion criteria. These studies provided 15 stress consequences and 20 stress factors. The most frequently reported stress factors were ‘contact with COVID-19 patients’, ‘no education or training in handling infectious diseases’ and ‘insufficient protective equipment’. Anxiety, stress, and depression were the most common outcomes identified. Analyses showed an increase in anxiety scores among HCWs who cared for COVID-19 patients, as well as a rise in depressive symptoms due to inadequate or no personal protective equipment. In this review, various pandemic-associated stress factors and stress consequences of healthcare workers were observed. With the results, criteria for effective measures and interventions can be developed to minimize the risk of stress consequences.

Integrative Brain Dynamics in Childhood Bullying Victimization: Cognitive and Emotional Convergence Associated With Stress Psychopathology.

Bullying victimization is a form of psychological stress that is associated with poor outcomes in the areas of mental health and learning. Although the emotional maladjustment and memory impairment following interpersonal stress are well documented, the mechanisms of complex cerebral dysfunctions have neither been outlined nor studied in depth in the context of childhood bullying victimization. As a contribution to the cross-disciplinary field of developmental psychology and neuroscience, we review the neuropathophysiology of early life stress, as well as general psychological stress to synthesize the data and clarify the versatile dynamics within neuronal networks linked to bullying victimization. The stress-induced neuropsychological cascade and associated cerebral networks with a focus on cognitive and emotional convergence are described. The main findings are that stress-evoked neuroendocrine reactivity relates to neuromodulation and limbic dysregulation that hinder emotion processing and executive functioning such as semantic cognition, cognitive flexibility, and learning. Developmental aspects and interacting neural mechanisms linked to distressed cognitive and emotional processing are pinpointed and potential theory-of-mind nuances in targets of bullying are presented. The results show that childhood stress psychopathology is associated with a complex interplay where the major role belongs to, but is not limited to, the amygdala, fusiform gyrus, insula, striatum, and prefrontal cortex. This interplay contributes to the sensitivity toward facial expressions, poor cognitive reasoning, and distress that affect behavioral modulation and emotion regulation. We integrate the data on major brain dynamics in stress neuroactivity that can be associated with childhood psychopathology to help inform future studies that are focused on the treatment and prevention of psychiatric disorders and learning problems in bullied children and adolescents.

Cytokines in the Brain and Neuroinflammation: We Didn't Starve the Fire!

In spite of the brain-protecting tissues of the skull, meninges, and blood-brain barrier, some forms of injury to or infection of the CNS can give rise to cerebral cytokine production and action and result in drastic changes in brain function and behavior. Interestingly, peripheral infection-induced systemic inflammation can also be accompanied by increased cerebral cytokine production. Furthermore, it has been recently proposed that some forms of psychological stress may have similar CNS effects. Different conditions of cerebral cytokine production and action will be reviewed here against the background of neuroinflammation. Within this context, it is important to both deepen our understanding along already taken paths as well as to explore new ways in which neural functioning can be modified by cytokines. This, in turn, should enable us to put forward different modes of cerebral cytokine production and action in relation to distinct forms of neuroinflammation.

The role of CXCL8 in chronic nonhealing diabetic foot ulcers and phenotypic changes in fibroblasts: a molecular perspective

A persistent inflammation is perpetuated by infiltrating immune cells and cytokines secreted from these immune cells. Additionally, apoptotic keratinocytes and adipocytes in diabetes causes diabetic foot ulcer (DFU) to arrest in an inflammatory phase without progressing to the resolution phase. This leads to a nonhealing DFU and, despite advanced treatments consisting of wound debridement, off-loading the ulcer of necrotic tissue, wound dressings to keep it moist and control exudate, medication, and preventing infection, DFUs remain a clinical problem. Nonhealing DFUs pose not only an economic burden but also increased morbidity and mortality in the form of psychological stress with and increased chance of amputation, and even death. Thus, investigating the complicated underlying molecular mechanism responsible for nonhealing patterns and designing better therapeutics is warranted. This review article focuses on the role of IL-8-mediated persistent inflammation and phenotypic change of fibroblasts due to this inflammatory cascade. We have discussed various sources of interleukin (IL)-8 secretion and the possible association of IL8-fibroblast plasticity as a cause of nonhealing DFUs. A literature search on PubMed, Google Scholar, and PMC was done including the terms diabetic foot ulcer, diabetes, diabetic ulcer, chronic inflammation, interleukin 8, diabetic wound, and nonhealing diabetic foot ulcers. The articles in the English language and published in last 10 years were selected. From the pool of these, the articles describing the relationship between IL-8 and nonhealing diabetic foot ulcer and diabetic ulcer were used sorted out and used for this review article following PRISMA guidelines. Increased infiltration of inflammatory immune cells, secretion of pro-inflammatory cytokines, altered keratinocyte-fibroblast function, and phenotypic changes of fibroblasts in DFUs seem to be critical to the nonhealing of DFUs. Thus, inhibiting IL-8 secretion and downstream signaling seems to be a goal of potential therapeutics.

Free Papers Compiled

Free Papers Compiled

Disproportionate Impacts of Wildfires among Elderly and Low-Income Communities in California from 2000-2020.

Wildfires can be detrimental to urban and rural communities, causing impacts in the form of psychological stress, direct physical injury, and smoke-related morbidity and mortality. This study examined the area burned by wildfires over the entire state of California from the years 2000 to 2020 in order to quantify and identify whether burned area and fire frequency differed across Census tracts according to socioeconomic indicators over time. Wildfire data were obtained from the California Fire and Resource Assessment Program (FRAP) and National Interagency Fire Center (NIFC), while demographic data were obtained from the American Community Survey. Results showed a doubling in the number of Census tracts that experienced major wildfires and a near doubling in the number of people residing in wildfire-impacted Census tracts, mostly due to an over 23,000 acre/year increase in the area burned by wildfires over the last two decades. Census tracts with a higher fire frequency and burned area had lower proportions of minority groups on average. However, when considering Native American populations, a greater proportion resided in highly impacted Census tracts. Such Census tracts also had higher proportions of older residents. In general, high-impact Census tracts tended to have higher proportions of low-income residents and lower proportions of high-income residents, as well as lower median household incomes and home values. These findings are important to policymakers and state agencies as it relates to environmental justice and the allocation of resources before, during, and after wildfires in the state of California.

GABAA Receptor Subtypes Regulate Stress-Induced Colon Inflammation in Mice

Psychological stress, in early life or adulthood, is a significant risk factor for inflammatory disorders, including inflammatory bowel diseases. However, little is known about the mechanisms by which emotional factors affect the immune system. γ-Aminobutyric acid type A receptors (GABAARs) regulate stress and inflammation, but it is not clear whether specific subtypes of GABAARs mediate stress-induced gastrointestinal inflammation. We investigated the roles of different GABAAR subtypes in mouse colon inflammation induced by 2 different forms of psychological stress. C57BL/6J mice were exposed to early-life stress, and adult mice were exposed to acute-restraint stress; control mice were not exposed to either form of stress. We collected colon tissues and measured contractility using isometric tension recordings; colon inflammation, based on levels of cluster of differentiation 163 and tumor necrosis factor messenger RNA (mRNA) and protein and myeloperoxidase activity; and permeability, based on levels of tight junction protein 1 and occludin mRNA and protein. Mice were given fluorescently labeled dextran orally and systemic absorption was measured. We also performed studies of mice with disruption of the GABAAR subunit α3 gene (Gabra3-/- mice). Mice exposed to early-life stress had significantly altered GABAAR-mediated colonic contractility and impaired barrier function, and their colon tissue had increased levels of Gabra3 mRNA compared with control mice. Restraint stress led to colon inflammation in C57/BL6J mice but not Gabra3-/- mice. Colonic inflammation was induced invitro by an α3-GABAAR agonist, showing a proinflammatory role for this receptor subtype. In contrast, α1/4/5-GABAAR ligands decreased the expression of colonic inflammatory markers. We found stress to increase expression of Gabra3 and induce inflammation in mouse colon, together with impaired barrier function. The invitro pharmacologic activation of α3-GABAARs recapitulated colonic inflammation, whereas α1/4/5-GABAAR ligands were anti-inflammatory. These proteins might serve as therapeutic targets for treatment of colon inflammation or inflammatory bowel diseases.

Total Phenolic Content of Ethanol Extract of Artrocarpus camansi Leave and its Effect to Superoxide Dismutase (SOD) Level in Mice

A free radical is one of the triggers of degenerative diseases that become the biggest cause of death. Excessive production of free radicals can be neutralized by antioxidant. Antioxidants can be generated from within the body (intracellular). One of them by the enzyme SOD (superoxide dismutase). However, when the production of free radicals exceeds the ability of intracellular antioxidants to neutralize it, antioxidants from outside (extracellular) is necessary. The ethanol extract of Artocarpus camansi leaves (EEACL) contains phenolic compounds which has very strong antioxidant activity based on in vitro study using the DPPH method, but the in vivo study about the total phenolic content effect of its leaves toward antioxidant activity has not been done. 25 mice were divided into 5 groups consisting of control group, a group was induced by stress and three groups were induced by stress, but given EEACL with each dose of 50 mg/kg bw, 100 mg/kg bw and 150 mg/kg bw. Inducing stress in the form of psychological stress was carried out for 7 days and continued with the EEACL administration for 7 days. The mice were dissected and the livers were isolated, then the liver morphological was examined using Hematoxyllin Eosin (HE) staining method and SOD level was examined with immunohistochemical staining method. The data were analyzed with One Way ANOVA and Duncan test using SPSS program version 19.0. Total phenolic content of EEACL is 235.03 ± 4.306 mg GAE/ g of sample. The average SOD levels in the control group is 94.05 %, stressed group is 55.94 %, stress with EEACL dose 50 mg/kg bw group is 58.40 %, stress with EEACL dose 100 mg/kg bw group is 79.68 %, stress with EEACL dose 150 mg/kg bw group is 80.90 %. Based on statistical result, SOD level increased along with the increase of EEACL dose, but not significantly (p < 0,05). Total phenolic content of EEACL has an influence to SOD levels. SOD level increased along with the increase of EEACL administration dose. The higher dose of EEACL leading to higher levels of SOD in the mouse liver.Keywords : total phenolic content, superoxide dismutase, antioxidant, Artocarpus camansi

Association of CD4+ T cell subpopulations and psychological stress measures in women living with HIV

ABSTRACTPsychological stress is a known immunomodulator. In individuals with HIV, depression, the most common manifestation of increased psychological stress, can affect immune function with lower CD4+ T cell counts correlating with higher levels of depression. It is unknown how other forms of psychological stress can impact immune markers in people living with HIV. We conducted a cross-sectional study to determine how CD4+ T cell subpopulations correlated with different forms of psychological stress. We recruited 50 HIV-positive women as part of the Women’s Interagency HIV Study. We assessed perceived stress, worry, acute anxiety, trait anxiety, and depression through self-report questionnaires and CD4+ T cell subpopulations using flow cytometry. Our sample was 96% African-American with a mean ± SD age and body mass index of 42 ± 8.8 years and 36.6 ± 11.5 kg/m2, respectively. The mean ± SD scores on the psychological measures were as follows: Perceived Stress Scale (PSS), 16.5 ± 6.4; Penn State Worry Questionnaire (PSWQ), 47.7 ± 13.8; State-Trait Anxiety Inventory – State (STAIS), 39.1 ± 12.3; State-Trait Anxiety Inventory – Trait (STAIT), 40.2 ± 11.4; Center for Epidemiological Studies Depression Scale (CES-D), 15.6 ± 11.4. The mean + SD values for the immune parameters were as follows: regulatory T cells (Treg), 1.25% ± 0.7; T helper 1 (Th1), 14.9% ± 6.1; T helper 2 (Th2), 3.8% ± 2; Th1/Th2 ratio, 4.6 ± 3; and CD4+ T cell count (cells/mm3), 493 ± 251. Treg levels positively correlated with PSS, STAIS, and STAIT. CD4+ T cell count negatively correlated with PSS, PSWQ, STAIS, STAIT, and CES-D. These data suggest that immune function may be impacted by various forms of psychological stress in HIV-positive women. Interventions that target stress reduction may be useful in improving immune parameters and quality of life.

Significance of Comorbid Psychological Stress and Depression on Outcomes After Cardiac Rehabilitation

BackgroundDepression is associated with increased mortality in stable coronary heart disease. Cardiac rehabilitation and exercise training has been shown to decrease depression, psychological stress, and mortality after a coronary heart disease event. The presence of depression at completion of cardiac rehabilitation and exercise training is associated with increased mortality. However, it is unknown if depression with comorbid psychological risk factors such as anxiety or hostility confers an additional mortality disadvantage. We evaluated the mortality effect of anxiety and hostility on depression after cardiac rehabilitation and exercise training. Patients and MethodsWe studied 1150 patients with coronary heart disease following major coronary heart disease events who had completed formal cardiac rehabilitation and exercise training. Using Kellner questionnaires, stress levels were measured in 1 of 3 domains: anxiety, hostility, and depression (with an aggregated overall psychological stress score) and divided into 3 groups: nondepressed (n = 1072), depression alone (n = 18), and depression with anxiety or hostility (n = 60). Subjects were analyzed for all-cause mortality over 161 months of follow-up (mean 6.4 years) by National Death Index. ResultsDepression after cardiac rehabilitation was not common (6.8%; mortality 20.8%) but when present, frequently associated with either anxiety or hostility (77% of depressed patients; mortality 22.0%). After adjustment for age, sex, ejection fraction, and baseline peak oxygen consumption, depression alone (hazard ratio [HR] 1.73, P = .04), as well as depression with comorbid psychological stress, was associated with higher mortality (HR 1.98, P = .03). Furthermore, our data showed an increased mortality when both anxiety and hostility were present in addition to depression after cardiac rehabilitation (HR 2.41, P = .04). ConclusionsAfter cardiac rehabilitation, depression, when present, is usually associated with other forms of psychological stress, which confers additional mortality. More measures are needed to address psychological stress after cardiac rehabilitation.

Relationships between Salivary Melatonin Levels, Quality of Sleep, and Stress in Young Japanese Females

A decrease in the quality of sleep is believed to cause anxiety and worsen depression. Comparisons of salivary melatonin levels with different factors including quality of sleep, state and trait anxieties, and depression, were conducted to examine whether there is a relationship between melatonin, presumably associated with sleep, and psychological stress. The saliva of healthy young females was collected during the daytime and before they went to bed at night (when they were awake and resting in a sitting position), and salivary melatonin levels were measured. The quality of sleep was scored using the Pittsburgh Sleep Quality Index (PSQI)—a questionnaire method. State and trait anxieties, and depression were scored using other questionnaire methods: the State-Trait Anxiety Inventory (STAI) and Self-Rating Depression Scale (SDS), respectively. The following findings were obtained: (1) Salivary melatonin levels measured during the daytime and before going to bed were higher in females with a high depression score, compared to those with a low score, and there was a correlation between the depression scores and salivary melatonin levels measured at night; and (2) salivary melatonin levels measured before going to bed at night (in a sitting position) were higher in females with a high state anxiety score, suggesting a correlation between state anxiety scores and salivary melatonin levels during the night. Both depression and a sense of anxiety are forms of psychological stress. Therefore, it is assumed that, when a person is under psychological stress, the action of melatonin as a ligand on its receptor is reduced. Meaning psychological stress may induce oxidative stress in the body. On the other hand, no correlation was noted between the quality of sleep and salivary melatonin levels during the night, presumably because saliva was collected when the subjects were awake and sitting, rather than sleeping.

Stress appraisals and cellular aging: A key role for anticipatory threat in the relationship between psychological stress and telomere length

Chronic psychological stress is a risk factor for multiple diseases of aging. Accelerated cellular aging as indexed by short telomere length has emerged as a potential common biological mechanism linking various forms of psychological stress and diseases of aging. Stress appraisals determine the degree and type of biological stress responses and altered stress appraisals may be a common psychological mechanism linking psychological stress and diseases of aging. However, no previous studies have examined the relationship between stress appraisals and telomere length. We exposed chronically stressed female caregivers and non-caregiving controls (N=50; M age=62.14±6.10) to a standardized acute laboratory stressor and measured their anticipatory and retrospective threat and challenge appraisals of the stressor. We hypothesized that threat and challenge appraisals would be associated with shorter and longer telomere length respectively, and that chronic caregiving stress would influence telomere length through altered stress appraisals. Higher anticipatory threat appraisals were associated with shorter age-adjusted telomere length (β=-.32, p=.03), but challenge appraisals and retrospective threat appraisals showed no independent association with telomere length. Caregivers reported significantly higher anticipatory (β=-.36, p=.006) and retrospective (β=-.29, p=.03) threat appraisals than controls, but similar challenge appraisals. Although there was no significant main effect of caregiver status on telomere length, caregiving had a significant indirect effect on telomere length through anticipatory threat appraisals. Exaggerated anticipatory threat appraisals may be a common and modifiable psychological mechanism of psychological stress effects on cellular aging.

Cardiovascular and behavioural responses to conditioned fear and restraint are not affected by retrograde lesions of A5 and C1 bulbospinal neurons

The aim of this study was to test a possible role of A5 neurons in the expression of the pressor and tachycardic responses to conditioned fear and restraint, two forms of psychological stress. Previous Fos studies have shown that the C1 adrenergic neurons and spinally projecting neurons in the vasopressor region of the rostral ventrolateral medulla are not activated by these two stressors, suggesting that these cardiovascular changes may be mediated by other premotor sympathetic (presympathetic) cell groups. The same studies also revealed that the A5 noradrenergic group was one of the main presympathetic cell groups to be activated in response to these two stressors. Thus, we hypothesized that the A5 group could mediate these cardiovascular responses. Conditioned fear and restraint were tested in rats implanted with radiotelemetric probes before and after retrograde lesion with the selective toxin anti-dopamine-β-hydroxylase-saporin bilaterally injected in the spinal cord at T2–T3. Six animals were selected that had the most extensive loss of spinally projecting catecholaminergic neurons: A5 (81%–95%) and rostral C1 (59%–86%, which would include most C1 bulbospinal neurons). However, despite this major loss of noradrenergic and adrenergic presympathetic neurons, the magnitude of the cardiovascular response to conditioned fear and restraint was the same before and after the lesion. Associated behavioural changes were not affected either. The results indicate that A5 presympathetic neurons are not essential for the expression of the tachycardic and pressor responses to conditioned fear and restraint. They also confirm that C1 bulbospinal neurons are not involved in these responses. The presympathetic neurons driving the tachycardic and pressor responses to conditioned fear and restraint must be elsewhere.

Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

As with other forms of psychological stress, conditioned fear causes an increase in body temperature. The mechanisms underlying this stress-induced hyperthermia are not well understood, but previous research suggests that nonshivering thermogenesis might contribute, as it does during cold exposure. The major source of nonshivering thermogenesis in the rat is brown adipose tissue (BAT), and the largest BAT deposit in that species is in the interscapular area just below the skin. BAT is also under sympathetic control via beta-adrenoceptors. If BAT contributes to fear-induced hyperthermia, then the interscapular skin should warm up faster than other skin areas, and this response should be suppressed by the beta-adrenoceptor antagonist, propranolol. We tested this noninvasively by infrared thermography. In conscious rats, 30 min of contextual fear caused hyperthermia (as indicated by a +1.5 degrees C increase in lumbar back skin temperature) and increased the difference in temperature between interscapular and lumbar back skin (TiScap - TBack) by +1 degrees C. Propranolol (10 mg/kg ip) completely abolished this hyperthermia; however, the TiScap-TBack increase was not reduced. In contrast, exposure to cold air (4 degrees C) induced a +2.7 degrees C increase in TiScap-TBack, which was reduced to +1 degrees C after propranolol. The results show that conditioned fear-induced hyperthermia is of nonshivering origin and mediated by beta-adrenoceptors, but interscapular BAT does not contribute to it and does not appear to be activated, either.

Differential effects of stress on escape and reflex responses to nociceptive thermal stimuli in the rat

Acute stress has been shown to increase latencies of nociceptive reflexes, and this effect is considered evidence for stress-induced analgesia. However, tests for nociception that rely on motivated operant escape assess cerebral processing of pain and could be modulated independent of reflex responses. We therefore compared the effects of an acute stressor (restraint) on escape responses and lick/guard reflexes to stimulation of the paws by a thermally regulated floor. Testing sessions included a pre-test exposure to 36 °C, followed by a test trial in which either escape from 44 or 36 °C or reflex responses to 44 °C were observed. Behavioral responses to stress were assessed during a three day period, with baseline testing on day 1, post-stress or control testing on day 2, and evaluation of long-term stress effects on day 3. On day 2, half the animals received 15 min of restraint stress, followed by 15-min pre-test and test trials. Licking and guarding responses to thermal stimulation during 44 °C test trials were significantly reduced by restraint stress, confirming previously reported stress effects on nociceptive reflexes. In contrast, learned escape responses to the same thermal stimulus were significantly enhanced after stress. The increase in operant sensitivity suggests that acute restraint, a form of psychological stress, produces hyperalgesia for a level of thermal stimulation that preferentially activates C nociceptors. These results are discussed in relation to studies involving physical or psychological forms of stress, different nociceptive stimuli, and assessment strategies used to evaluate thermal pain sensitivity.

Enhancement of delayed release of dopamine in the amygdala induced by conditioned fear stress in methamphetamine-sensitized rats

Behavior during conditioned fear stress, a form of psychological stress, and the release of dopamine in the amygdala were measured over time using methamphetamine-sensitized rats, which are considered to be a model of hypersensitivity and vulnerability to emotional stress associated with stimulant-induced psychosis and schizophrenia. Dopamine release in the amygdala showed a delayed increase following completion of freezing behavior induced by conditioned fear stress regardless of the presence or absence of methamphetamine-sensitization. Since methamphetamine treatment did not lower the basal level of dopamine in the amygdala, under the conditions of this study, methamphetamine was presumed not to show neurotoxicity. On the other hand, basal dopamine levels after 15 h of repeated electric foot shock were about 40% lower than those in the control group ( p<0.0002). In addition, dopamine release following conditioned fear stress in animals repeatedly treated with methamphetamine increased significantly from 40 to 100 min after conditioned fear stress while the duration of freezing behavior or latency of the appearance of grooming were not different from those in the control group. The above results suggested that delayed dopamine release in the amygdala is a phenomenon strongly associated with the emotional context of conditioned fear stress, and hypersensitivity and vulnerability to stress are at least partially involved with the overreaction to stress.