Understanding and targeting dynamic stress responses of the brain: What we have learned and how to improve neurocognitive outcome following neurotoxic insult

2016 ◽  
Vol 57 (5) ◽  
pp. 319-321
Author(s):  
Charles L. Limoli
Keyword(s):  
Stress Responses ◽  
Dynamic Stress ◽  
Neurocognitive Outcome ◽  
The Brain

Insights into the molecular basis of host behaviour manipulation by Toxoplasma gondii infection

2017 ◽  
Vol 1 (6) ◽  
pp. 563-572 ◽  
Author(s):  
Pierre-Mehdi Hammoudi ◽  
Dominique Soldati-Favre
Keyword(s):  
Toxoplasma Gondii ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Brain Regions ◽  
Intermediate Hosts ◽  
Toxoplasma Gondii Infection ◽  
Host Parasite ◽  
Host Behaviour ◽  
The Brain ◽  
Brain Homeostasis

Typically illustrating the ‘manipulation hypothesis’, Toxoplasma gondii is widely known to trigger sustainable behavioural changes during chronic infection of intermediate hosts to enhance transmission to its feline definitive hosts, ensuring survival and dissemination. During the chronic stage of infection in rodents, a variety of neurological dysfunctions have been unravelled and correlated with the loss of cat fear, among other phenotypic impacts. However, the underlying neurological alteration(s) driving these behavioural modifications is only partially understood, which makes it difficult to draw more than a correlation between T. gondii infection and changes in brain homeostasis. Moreover, it is barely known which among the brain regions governing fear and stress responses are preferentially affected during T. gondii infection. Studies aiming at an in-depth dissection of underlying molecular mechanisms occurring at the host and parasite levels will be discussed in this review. Addressing this reminiscent topic in the light of recent technical progress and new discoveries regarding fear response, olfaction and neuromodulator mechanisms could contribute to a better understanding of this complex host–parasite interaction.

Mineralocorticoid Receptors and Glucocorticoid Receptors in HPA Stress Responses During Coping and Adaptation

2020 ◽  
Author(s):  
Edo Ronald de Kloet ◽  
Marian Joëls
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Coping Style ◽  
Glucocorticoid Receptors ◽  
Memory Storage ◽  
Salt Appetite ◽  
Mineralocorticoid Receptors ◽  
Stress Response System ◽  
Appraisal Processes ◽  
The Brain

The glucocorticoid hormones cortisol and corticosterone coordinate circadian events and are master regulators of the stress response. These actions of the glucocorticoids are mediated by mineralocorticoid receptors (NR3C2, or MRs) and glucocorticoid receptors (NR3C1, or GRs). MRs bind the natural glucocorticoids cortisol and corticosterone with a 10-fold higher affinity than GRs. The glucocorticoids are inactivated only in the nucleus tractus solitarii (NTS), rendering the NTS-localized MRs aldosterone-selective and involved in regulation of salt appetite. Everywhere else in the brain MRs are glucocorticoid-preferring. MR and GR are transcription factors involved in gene regulation but recently were also found to mediate rapid non-genomic actions. Genomic MRs, with a predominant localization in limbic circuits, are important for the threshold and sensitivity of the stress response system. Non-genomic MRs promote appraisal processes, memory retrieval, and selection of coping style. Activation of GRs makes energy substrates available and dampens initial defense reactions. In the brain, GR activation enhances appetitive- and fear-motivated behavior and promotes memory storage of the selected coping style in preparation of the future. Thus, MRs and GRs complement each other in glucocorticoid control of the initiation and termination of the stress response, suggesting that the balance in MR- and GR-mediated actions is crucial for homeostasis and health.

Stimuli and consequences of dendritic release of oxytocin within the brain

2007 ◽  
Vol 35 (5) ◽  
pp. 1252-1257 ◽  
Author(s):  
I.D. Neumann
Keyword(s):  
Paraventricular Nucleus ◽  
Stress Responses ◽  
Supraoptic Nucleus ◽  
Brain Regions ◽  
Model System ◽  
Intracerebral Microdialysis ◽  
Psychotherapeutic Intervention ◽  
Psychiatric Illnesses ◽  
Oxytocin Release ◽  
The Brain

The brain oxytocin system has served as a distinguished model system in neuroendocrinology to study detailed mechanisms of intracerebral release, in particular of somatodendritic release, and its behavioural and neuroendocrine consequences. It has been shown that oxytocin is released within various brain regions, but evidence for dendritic release is limited to the main sites of oxytocin synthesis, i.e. the hypothalamic SON (supraoptic nucleus) and PVN (paraventricular nucleus). In the present paper, stimuli of dendritic release of oxytocin and the related neuropeptide vasopressin are discussed, including parturition and suckling, i.e. the period of a highly activated brain oxytocin system. Also, exposure to various pharmacological, psychological or physical stressors triggers dendritic oxytocin release, as monitored by intracerebral microdialysis within the SON and PVN during ongoing behavioural testing. So far, dendritic release of the neuropeptide has only been demonstrated within the hypothalamus, but intracerebral oxytocin release has also been found within the central amygdala and the septum in response to various stimuli including stressor exposure. Such a locally released oxytocin modulates physiological and behavioural reproductive functions, emotionality and hormonal stress responses, as it exerts, for example, pro-social, anxiolytic and antistress actions within restricted brain regions. These discoveries make oxytocin a promising neuromodulator of the brain for psychotherapeutic intervention and treatment of numerous psychiatric illnesses, for example, anxiety-related diseases, social phobia, autism and postpartum depression.

Regulation by protein tyrosine phosphorylation of stress responses in the brain

2010 ◽  
Vol 68 ◽  
pp. e58
Author(s):  
Hiroshi Ohnishi ◽  
Shinya Kusakari ◽  
Takaaki Murata ◽  
Toshi Maruyama ◽  
Yuriko Hayashi ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Stress Responses ◽  
Protein Tyrosine Phosphorylation ◽  
Protein Tyrosine ◽  
The Brain

Transient Process Response Analysis of Forced Synchronous Elliptical Vibrating Screen

2010 ◽  
Vol 118-120 ◽  
pp. 962-966
Author(s):  
Lian Wan Zhang ◽  
Zhong Jun Yin ◽  
Xin Sun ◽  
Zhi Chao Tang
Keyword(s):  
Steady State ◽  
Harmonic Analysis ◽  
Transient Process ◽  
Stress Level ◽  
Stress Responses ◽  
Large Scale ◽  
Dynamic Stress ◽  
Response Analysis ◽  
Vibrating Screen ◽  
Existing Structure

This paper is based on the scientific modeling of large-scale elliptical vibrating screen which is widely used in many fields. Through the tool of harmonic analysis in ANSYS, the dynamic stress responses during steady state and transient process are studied. The results confirmed that the existing structure can fulfill the requirement of dynamic stress level. Another contribution of this paper is to provide a new idea to analyze the transient process response, especially when the motor data are not sure.

scholarly journals Proteomic Analysis of Hydromethylthionine in the Line 66 Model of Frontotemporal Dementia Demonstrates Actions on Tau-Dependent and Tau-Independent Networks

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2162
Author(s):  
Karima Schwab ◽  
Valeria Melis ◽  
Charles R. Harrington ◽  
Claude M. Wischik ◽  
Mandy Magbagbeolu ◽  
...  
Keyword(s):  
Frontotemporal Dementia ◽  
Stress Responses ◽  
Protein Ubiquitination ◽  
Brain Proteome ◽  
Homeostatic Function ◽  
Behavioural Phenotypes ◽  
Tau Aggregation ◽  
The Brain ◽  
Key Pathways ◽  
Dimensional Electrophoresis

Abnormal aggregation of tau is the pathological hallmark of tauopathies including frontotemporal dementia (FTD). We have generated tau-transgenic mice that express the aggregation-prone P301S human tau (line 66). These mice present with early-onset, high tau load in brain and FTD-like behavioural deficiencies. Several of these behavioural phenotypes and tau pathology are reversed by treatment with hydromethylthionine but key pathways underlying these corrections remain elusive. In two proteomic experiments, line 66 mice were compared with wild-type mice and then vehicle and hydromethylthionine treatments of line 66 mice were compared. The brain proteome was investigated using two-dimensional electrophoresis and mass spectrometry to identify protein networks and pathways that were altered due to tau overexpression or modified by hydromethylthionine treatment. Overexpression of mutant tau induced metabolic/mitochondrial dysfunction, changes in synaptic transmission and in stress responses, and these functions were recovered by hydromethylthionine. Other pathways, such as NRF2, oxidative phosphorylation and protein ubiquitination were activated by hydromethylthionine, presumably independent of its function as a tau aggregation inhibitor. Our results suggest that hydromethylthionine recovers cellular activity in both a tau-dependent and a tau-independent fashion that could lead to a wide-spread improvement of homeostatic function in the FTD brain.

Trauma-Informed Practice for Pre-service Teachers

2019 ◽  
Author(s):  
Carmel Hobbs ◽  
Dane Paulsen ◽  
Jeff Thomas
Keyword(s):  
Stress Responses ◽  
Attachment Styles ◽  
Complex Trauma ◽  
Initial Teacher Education ◽  
Multidisciplinary Teams ◽  
Substantial Impact ◽  
Trauma Informed ◽  
Negative Impacts ◽  
Trauma Informed Practice ◽  
The Brain

Complex trauma experienced in childhood has detrimental impacts on the brain, learning and socio-moral development, the effects of which can last long into adulthood. A growing body of research emphasizes how all school teachers, regardless of the educational context, should expect to have students in their classroom who are affected by complex trauma. Teachers therefore require an understanding of how trauma affects their students, and a skillset that allows them to support and respond effectively to these students. However, multiple studies have found that teachers feel that they have not received sufficient training, and subsequently feel inadequately equipped to meet the needs of trauma-affected students in their classrooms. Although many Initial Teacher Education programs incorporate some curriculum on child maltreatment, this is typically focused on identifying and reporting child abuse, as opposed to how sustained and severe maltreatment can lead to complex trauma, which affects learning, and social development in students. Increasing understanding of how trauma affects the brain, and the implications this has for young people in school has continued to grow since the 1990s. This has contributed to a growing trend of multidisciplinary teams combining education and wellbeing models in schools to cater to the most vulnerable students in their respective communities. Students who have experienced trauma may appear to be deliberately misbehaving in the classroom, disengaged or disinterested in learning, and can struggle to develop skills that strengthen positive relationships with school staff and other students. Unsurprisingly, exposure to trauma impacts a young person’s academic performance, attendance, and likelihood of completion. It is clear that schools are important settings where the effects of trauma have a substantial impact on the lives of students, particularly when the effects of trauma are misunderstood. Nevertheless, schools have the potential to be one of the most powerful places for buffering the negative impacts of complex childhood trauma through their capacity to provide opportunities for all students to experience positive, trusting relationships, be cared for, and experience predictability, consistency and safety. A trauma-informed approach in school settings involves understanding how trauma affects students and provides a framework for responding to students rather than blaming them for their behavior. Trauma-informed practice is not an intervention, and it does not have an end point. It is a process, and a holistic way of working that involves understanding and attending to the specific needs of individuals with trauma-affected childhoods. Central to all trauma-informed approaches is the importance of strong, trusting, consistent and predictable relationships between an adult and a trauma-affected child. It is within this space that opportunities to repair dysregulated stress responses, and disruptive attachment styles can take place.

scholarly journals Glucagon-Like Peptide-1 (GLP-1) in the Integration of Neural and Endocrine Responses to Stress

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3304
Author(s):  
Yolanda Diz-Chaves ◽  
Salvador Herrera-Pérez ◽  
Lucas C. González-Matías ◽  
José Antonio Lamas ◽  
Federico Mallo
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Stress Responses ◽  
Food Motivation ◽  
Hedonic Value ◽  
Central Actions ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Second Messenger Pathways ◽  
The Brain

Glucagon like-peptide 1 (GLP-1) within the brain is produced by a population of preproglucagon neurons located in the caudal nucleus of the solitary tract. These neurons project to the hypothalamus and another forebrain, hindbrain, and mesolimbic brain areas control the autonomic function, feeding, and the motivation to feed or regulate the stress response and the hypothalamic-pituitary-adrenal axis. GLP-1 receptor (GLP-1R) controls both food intake and feeding behavior (hunger-driven feeding, the hedonic value of food, and food motivation). The activation of GLP-1 receptors involves second messenger pathways and ionic events in the autonomic nervous system, which are very relevant to explain the essential central actions of GLP-1 as neuromodulator coordinating food intake in response to a physiological and stress-related stimulus to maintain homeostasis. Alterations in GLP-1 signaling associated with obesity or chronic stress induce the dysregulation of eating behavior. This review summarized the experimental shreds of evidence from studies using GLP-1R agonists to describe the neural and endocrine integration of stress responses and feeding behavior.

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