Don't Stress, It's Under Control: Neural Correlates of Stressor Controllability in Humans

Animal research has repeatedly shown that experience of control over an aversive event can protect against the negative consequences of later uncontrollable stress. Neurobiologically, this effect is assumed to correspond to persistent changes in the pathway linking the ventromedial prefrontal cortex (vmPFC) and the dorsal raphe nucleus. However, it remains unclear to what extent these findings translate to humans. During functional magnetic resonance imaging, we subjected participants to controllable and uncontrollable aversive but non-painful electric stimuli, as well as to a control condition without aversive stimulation. In each trial, a symbol signalled whether participants could terminate the stressor through correct performance in a button-matching task or whether the stressor would be randomly terminated, i.e., uncontrollable. Along with neural responses, we assessed participants' accuracy, reaction times, and heart rate. To relate neural activations and subjective experience, we asked participants to rate perceived control, helplessness, and stress. Results were largely in line with our hypotheses. The vmPFC was generally deactivated by stress, but this effect was attenuated when participants could terminate the stressor compared to when their responses had no effect. Furthermore, activation in stress-responsive regions, including the bilateral insula, was reduced during controllable trials. Under uncontrollable stress, greater vmPFC recruitment was linked to reduced feelings of helplessness. An investigation of condition-dependent differences in vmPFC connectivity yielded no significant results. Our findings further corroborate animal research and emphasise the role of the vmPFC in controllability-dependent regulation of stress responses. Based on the results, we discuss future directions in the context of resilience research and mental health promotion.

Metacognition, Stress – Relaxation Balance & Related Hormones

This paper examines the interaction between metacognition and stress response. Specifically, the main purpose of this study is to trace the interaction between metacognition, sympathetic-parasympathetic nervous system and the basic stress-related hormones/neurotransmitters. To achieve this aim, the research seeks to address the following questions: Can metacognition regulate the stress-related hormones and the sympathetic nervous system hyperactivity? How can it contribute to the regulation of uncontrollable stress? What is the role of executive functions? Can metacognition stop the cells and neurons from degeneration and the brain from shrinking? The evidence support the hypothesis that there is a deep relationship between metacognition, stress-related hormones and autonomic nervous system. Therefore, the above finding paves the way for the design of new stress management strategies, which could implemented in family, in school and in workplace. Uncontrollable stress constitutes the “health epidemic” of our century. Mental and mood disorders, premature ageing, cognitive impairments, learning disabilities are some of the stress-related threats. There is an urgent need to focus on resilience in order to cope with stress and to stay in balance.

PENERAPAN TEKNIK RELAKSASI DISELA PENGERJAAN TUGAS OLEH MAHASISWA DIMASA COVID-19

ABSTRAK Pandemi civid-19 pada masa sekarang menyebabkan semua serba onlen termasuk pengerjaan tugas yang membuat para dosen mengira bahwasanya di rumah saja hanya rebahan dan tidak melakukan aktivitas yang membuat banyaknya tugas yang di berikan oleh mahasiswa, hal ini menyebabkan mahasiswa banyak mengalami stress yang tidak terkendali, emosi yang tidak stabil, tekanan fikiran, perubahan perilaku mahasiswa. Hal ini banyak sekali terjadi di masa pandemic covid-19 ini. Yang kemudian diperlukannya tips – tips untuk menjadi penerapan yang bisa di lakukan di masa pandemic covid-19 yang mengharuskan mahasiswa beraktivitas di rumah saja. Beberapa tips yang bisa dilakukan mahasiswa selama di rumah saja seperti relaksasi nafas, relaksasi imagery, mendengarkan musik, serta rehat sejenak untuk mengerjakan tugas dan kemudian dilanjutkan kembali, hal ini bisa menjadi jalan keluar bagi mahasiswa yang sedang mengalami tekanan, jenuh dan stress dikala pengerjaan tugas dan terbukti efektif. Kata Kunci : mahasiswa, relaksasi, pandemi covid-19 ABSTRACTThe Civid-19 pandemic at the present time causes everything to be online, including work on assignments that make lecturers think that at home, they are just lying down and not doing activities that cause many assignments given by students, this causes students to experience a lot of uncontrollable stress, unstable emotions, stress, changes in student behavior. This happened a lot during the Covid-19 pandemic. What then needs tips to become an application that can be done during the Covid-19 pandemic, which requires students to do activities at home. Some tips that students can do while at home such as breathing relaxation, imagery relaxation, listening to music, and taking a break to do assignments and then continuing again, this can be a way out for students who are experiencing pressure, boredom and stress while doing assignments and proven effective.Keywords ; Collage Student, relaxtion, the covid-19 pandemic

Chronic Stress Weakens Connectivity in the Prefrontal Cortex: Architectural and Molecular Changes

Chronic exposure to uncontrollable stress causes loss of spines and dendrites in the prefrontal cortex (PFC), a recently evolved brain region that provides top-down regulation of thought, action, and emotion. PFC neurons generate top-down goals through recurrent excitatory connections on spines. This persistent firing is the foundation for higher cognition, including working memory, and abstract thought. However, exposure to acute uncontrollable stress drives high levels of catecholamine release in the PFC, which activates feedforward calcium-cAMP signaling pathways to open nearby potassium channels, rapidly weakening synaptic connectivity to reduce persistent firing. Chronic stress exposures can further exacerbate these signaling events leading to loss of spines and resulting in marked cognitive impairment. In this review, we discuss how stress signaling mechanisms can lead to spine loss, including changes to BDNF-mTORC1 signaling, calcium homeostasis, actin dynamics, and mitochondrial actions that engage glial removal of spines through inflammatory signaling. Stress signaling events may be amplified in PFC spines due to cAMP magnification of internal calcium release. As PFC dendritic spine loss is a feature of many cognitive disorders, understanding how stress affects the structure and function of the PFC will help to inform strategies for treatment and prevention.

A Translational Paradigm to Study the Effects of Uncontrollable Stress in Humans

Theories on the aetiology of depression in humans are intimately linked to animal research on stressor controllability effects. However, explicit translations of established animal designs are lacking. In two consecutive studies, we developed a translational paradigm to study stressor controllability effects in humans. In the first study, we compared three groups of participants, one exposed to escapable stress, one yoked inescapable stress group, and a control group not exposed to stress. Although group differences indicated successful stress induction, the manipulation failed to differentiate groups according to controllability. In the second study, we employed an improved paradigm and contrasted only an escapable stress group to a yoked inescapable stress group. The final design successfully induced differential effects on self-reported perceived control, exhaustion, helplessness, and behavioural indices of adaptation to stress. The latter were examined in a new escape behaviour test which was modelled after the classic shuttle box animal paradigm. Contrary to the learned helplessness literature, exposure to uncontrollable stress led to more activity and exploration; however, these behaviours were ultimately not adaptive. We discuss the results and possible applications in light of the findings on learning and agency beliefs, inter-individual differences, and interventions aimed at improving resilience to stress-induced mental dysfunction.

Attachment Security Moderates Effects of Uncontrollable Stress on Preadolescent Hypothalamic–Pituitary–Adrenal Axis Responses: Evidence of Regulatory Fit

This study examined whether perceived attachment security (i.e., perceptions of caregivers as responsive, available, and open to communication during times of need) and effortful coping work in concert to buffer against uncontrollable life event effects on hypothalamic–pituitary–adrenal axis (HPA) response patterns in preadolescent boys and girls ( N = 121, mean age = 10.60 years). Children completed the Trier Social Stress Test (TSST) and were immediately thereafter exposed to one of two randomly assigned coping conditions: distraction and avoidance. Piecewise growth multilevel modeling of children’s salivary cortisol levels over the course of the experimental protocol suggested that uncontrollable life events in the year prior were associated with exaggerated cortisol reactivity, though this pattern was buffered against by children’s secure attachment beliefs. Furthermore, perceived attachment security, uncontrollable life event, and coping condition interactive effects on cortisol recovery emerged. As expected, distraction supported efficient cortisol recovery for those uncontrollable stress-exposed children with secure beliefs, and avoidance worked in this fashion for those with insecure beliefs. Findings point to perceived attachment security as a putative buffer of stress-exposed preadolescents’ HPA reactivity and possible contributor to regulatory fit, informing how specific coping skills work or backfire in supporting these children’s HPA recovery efficiency.

Loss of Prefrontal Cortical Higher Cognition with Uncontrollable Stress: Molecular Mechanisms, Changes with Age, and Relevance to Treatment

The newly evolved prefrontal cortex (PFC) generates goals for “top-down” control of behavior, thought, and emotion. However, these circuits are especially vulnerable to uncontrollable stress, with powerful, intracellular mechanisms that rapidly take the PFC “off-line.” High levels of norepinephrine and dopamine released during stress engage α1-AR and D1R, which activate feedforward calcium-cAMP signaling pathways that open nearby potassium channels to weaken connectivity and reduce PFC cell firing. Sustained weakening with chronic stress leads to atrophy of dendrites and spines. Understanding these signaling events helps to explain the increased susceptibility of the PFC to stress pathology during adolescence, when dopamine expression is increased in the PFC, and with advanced age, when the molecular “brakes” on stress signaling are diminished by loss of phosphodiesterases. These mechanisms have also led to pharmacological treatments for stress-related disorders, including guanfacine treatment of childhood trauma, and prazosin treatment of veterans and civilians with post-traumatic stress disorder.