Hippocampal BDNF in physiological conditions and social isolation

2017 ◽  
Vol 28 (6) ◽  
pp. 675-692 ◽  
Author(s):  
Ivan Zaletel ◽  
Dragana Filipović ◽  
Nela Puškaš
Keyword(s):  
Psychiatric Disorders ◽  
Social Isolation ◽  
Intracellular Signaling ◽  
Social Stress ◽  
Current Knowledge ◽  
Bdnf Expression ◽  
Physiological Conditions ◽  
Age Dependent ◽  
Chronic Psychosocial Stress ◽  
Pituitary Adrenal Axis

AbstractExposure of an organism to chronic psychosocial stress may affect brain-derived neurotrophic factor (BDNF) expression that has been implicated in the etiology of psychiatric disorders, such as depression. Given that depression in humans has been linked with social stress, the chronic social stress paradigms for modeling psychiatric disorders in animals have thus been developed. Chronic social isolation in animal models generally causes changes in hypothalamic-pituitary-adrenal axis functioning, associated with anxiety- and depressive-like behaviors. Also, this chronic stress causes downregulation of BDNF protein and mRNA in the hippocampus, a stress-sensitive brain region closely related to the pathophysiology of depression. In this review, we discuss the current knowledge regarding the structure, function, intracellular signaling, inter-individual differences and epigenetic regulation of BDNF in both physiological conditions and depression and changes in corticosterone levels, as a marker of stress response. Since BDNF levels are age dependent in humans and rodents, this review will also highlight the effects of adolescent and adult chronic social isolation models of both genders on the BDNF expression.

scholarly journals The physiology of regulated BDNF release

2020 ◽  
Vol 382 (1) ◽  
pp. 15-45 ◽  
Author(s):  
Tanja Brigadski ◽  
Volkmar Leßmann
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Detailed Knowledge ◽  
Cellular Regulation ◽  
Bdnf Expression ◽  
Physiological Conditions ◽  
Brain Circuits ◽  
Important Regulator ◽  
Network Plasticity ◽  
The Brain

Abstract The neurotrophic factor BDNF is an important regulator for the development of brain circuits, for synaptic and neuronal network plasticity, as well as for neuroregeneration and neuroprotection. Up- and downregulations of BDNF levels in human blood and tissue are associated with, e.g., neurodegenerative, neurological, or even cardiovascular diseases. The changes in BDNF concentration are caused by altered dynamics in BDNF expression and release. To understand the relevance of major variations of BDNF levels, detailed knowledge regarding physiological and pathophysiological stimuli affecting intra- and extracellular BDNF concentration is important. Most work addressing the molecular and cellular regulation of BDNF expression and release have been performed in neuronal preparations. Therefore, this review will summarize the stimuli inducing release of BDNF, as well as molecular mechanisms regulating the efficacy of BDNF release, with a focus on cells originating from the brain. Further, we will discuss the current knowledge about the distinct stimuli eliciting regulated release of BDNF under physiological conditions.

scholarly journals Neuroimmunological Responses to Social Isolation

2015 ◽  
Vol 17 (1) ◽  
pp. 10 ◽  
Author(s):  
Karol Ramirez DDS, MSc, PhD
Keyword(s):  
Social Isolation ◽  
Social Stress ◽  
Inflammatory Diseases ◽  
Psychosocial Stressors ◽  
Future Research ◽  
Chronic Activation ◽  
New Perspective ◽  
Underlying Mechanisms ◽  
Perceived Social Isolation ◽  
Pituitary Adrenal Axis

Objective social isolation and perceived social isolation are psychosocial stressors that may impair the normal functioning of the neuroimmune system. Chronic activation of the neuro-immuno-endocrine communication and the consequent loss of homeostasis may lead to the appearance of pathologies and associated mood disorders. For example, alterations in the hypothalamic-pituitary- adrenal axis and sympathetic nervous system dynamics may account for the observed predisposition to inflammatory diseases following chronic social stress. Therefore, it is necessary to further study the underlying mechanisms in social isolation in order to prevent its deleterious effects on health. The objective of this New Perspective article is to supplement the understanding of the neuroimmunological responses to social isolation and provide a basis for future research in this topic. 

scholarly journals The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Li Ning ◽  
Xiong Rui ◽  
Wang Bo ◽  
Geng Qing
Keyword(s):  
Histone Deacetylase ◽  
Chromatin Remodeling ◽  
Current Knowledge ◽  
Organ Injury ◽  
Solid Organ ◽  
Solid Organ Injury ◽  
Histone Deacetylase 3 ◽  
Physiological Conditions ◽  
Inflammatory Conditions ◽  
Therapeutic Value

AbstractHistone deacetylase 3 (HDAC3) plays a crucial role in chromatin remodeling, which, in turn, regulates gene transcription. Hence, HDAC3 has been implicated in various diseases, including ischemic injury, fibrosis, neurodegeneration, infections, and inflammatory conditions. In addition, HDAC3 plays vital roles under physiological conditions by regulating circadian rhythms, metabolism, and development. In this review, we summarize the current knowledge of the physiological functions of HDAC3 and its role in organ injury. We also discuss the therapeutic value of HDAC3 in various diseases.

scholarly journals Suprabasin—A Review

Genes ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 108
Author(s):  
Miroslav Pribyl ◽  
Zdenek Hodny ◽  
Iva Kubikova
Keyword(s):  
Glioblastoma Multiforme ◽  
Poor Prognosis ◽  
Current Knowledge ◽  
Original Description ◽  
Oesophageal Carcinoma ◽  
Secreted Proteins ◽  
Cornified Envelope ◽  
Physiological Conditions ◽  
Signalling Molecules ◽  
Human Genes

Among the ~22,000 human genes, very few remain that have unknown functions. One such example is suprabasin (SBSN). Originally described as a component of the cornified envelope, the function of stratified epithelia-expressed SBSN is unknown. Both the lack of knowledge about the gene role under physiological conditions and the emerging link of SBSN to various human diseases, including cancer, attract research interest. The association of SBSN expression with poor prognosis of patients suffering from oesophageal carcinoma, glioblastoma multiforme, and myelodysplastic syndromes suggests that SBSN may play a role in human tumourigenesis. Three SBSN isoforms code for the secreted proteins with putative function as signalling molecules, yet with poorly described effects. In this first review about SBSN, we summarised the current knowledge accumulated since its original description, and we discuss the potential mechanisms and roles of SBSN in both physiology and pathology.

scholarly journals Dual-Specificity, Tyrosine Phosphorylation-Regulated Kinases (DYRKs) and cdc2-Like Kinases (CLKs) in Human Disease, an Overview

2021 ◽  
Vol 22 (11) ◽  
pp. 6047
Author(s):  
Mattias F. Lindberg ◽  
Laurent Meijer
Keyword(s):  
Tyrosine Phosphorylation ◽  
Human Disease ◽  
Intracellular Signaling ◽  
Neuronal Development ◽  
Viral Infections ◽  
Current Knowledge ◽  
Lymphoblastic Leukemia ◽  
Cell Cycle Control ◽  
Megakaryoblastic Leukemia ◽  
Dual Specificity

Dual-specificity tyrosine phosphorylation-regulated kinases (DYRK1A, 1B, 2-4) and cdc2-like kinases (CLK1-4) belong to the CMGC group of serine/threonine kinases. These protein kinases are involved in multiple cellular functions, including intracellular signaling, mRNA splicing, chromatin transcription, DNA damage repair, cell survival, cell cycle control, differentiation, homocysteine/methionine/folate regulation, body temperature regulation, endocytosis, neuronal development, synaptic plasticity, etc. Abnormal expression and/or activity of some of these kinases, DYRK1A in particular, is seen in many human nervous system diseases, such as cognitive deficits associated with Down syndrome, Alzheimer’s disease and related diseases, tauopathies, dementia, Pick’s disease, Parkinson’s disease and other neurodegenerative diseases, Phelan-McDermid syndrome, autism, and CDKL5 deficiency disorder. DYRKs and CLKs are also involved in diabetes, abnormal folate/methionine metabolism, osteoarthritis, several solid cancers (glioblastoma, breast, and pancreatic cancers) and leukemias (acute lymphoblastic leukemia, acute megakaryoblastic leukemia), viral infections (influenza, HIV-1, HCMV, HCV, CMV, HPV), as well as infections caused by unicellular parasites (Leishmania, Trypanosoma, Plasmodium). This variety of pathological implications calls for (1) a better understanding of the regulations and substrates of DYRKs and CLKs and (2) the development of potent and selective inhibitors of these kinases and their evaluation as therapeutic drugs. This article briefly reviews the current knowledge about DYRK/CLK kinases and their implications in human disease.

scholarly journals Interindividual variability and lateralization of µ-opioid receptors in the human brain

2019 ◽  
Author(s):  
Tatu Kantonen ◽  
Tomi Karjalainen ◽  
Janne Isojärvi ◽  
Pirjo Nuutila ◽  
Jouni Tuisku ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Body Mass ◽  
Opioid Receptors ◽  
Hierarchical Modeling ◽  
Small Sample ◽  
Hemispheric Lateralization ◽  
Binding Potential ◽  
Neuropsychiatric Diseases ◽  
Age Dependent

AbstractThe brain’s µ-opioid receptors (MORs) are involved in analgesia, reward and mood regulation. Several neuropsychiatric diseases have been associated with dysfunctional MOR system, and there is also considerable variation in receptor density among healthy individuals. Sex, age, body mass and smoking have been proposed to influence the MOR system, but due to small sample sizes the magnitude of their influence remains inconclusive. Here we quantified in vivo MOR availability in the brains of 204 individuals with no neurologic or psychiatric disorders using positron emission tomography (PET) with tracer [11C]carfentanil. We then used Bayesian hierarchical modeling to estimate the effects of sex, age, body mass index (BMI) and smoking on [11C]carfentanil binding potential. We also examined hemispheric lateralization of MOR availability. Age had regionally specific effects on MOR availability, with age-dependent increase in frontotemporal areas but decrease in amygdala, thalamus, and nucleus accumbens. The age-dependent increase was stronger in males. MOR availability was globally lowered in smokers but independent of BMI. Finally, MOR availability was higher in the right versus the left hemisphere. The presently observed variation in MOR availability may explain why some individuals are prone to develop MOR-linked pathological states, such as chronic pain or psychiatric disorders.

Lacticaseibacillus paracasei NK112 mitigates Escherichia coli-induced depression and cognitive impairment in mice by regulating IL-6 expression and gut microbiota

2021 ◽  
pp. 1-12
Author(s):  
S.-W. Yun ◽  
J.-K. Kim ◽  
M.J. Han ◽  
D.-H. Kim
Keyword(s):  
Escherichia Coli ◽  
Cognitive Impairment ◽  
Gut Microbiota ◽  
Psychiatric Disorders ◽  
Myeloperoxidase Activity ◽  
Bdnf Expression ◽  
Strain Collection ◽  
Tnf Α ◽  
Faecal Bacteria ◽  
Anxiety Depression

The gut microbiota communicates with the brain through microbiota-gut-brain (MGB) and hypothalamus-pituitary-adrenal (HPA) axes and other pathways. Excessive expression of interleukin (IL)-6 is closely associated with the occurrence of the psychiatric disorders depression and dementia. Therefore, to understand whether IL-6 expression-suppressing probiotics could alleviate psychiatric disorders, we isolated IL-6 expression-inhibiting Lacticaseibacillus paracasei (formerly Lactobacillus paracasei) NK112 from the human faecal bacteria strain collection (Neurobiota Research Center, Seoul, Korea) and examined its therapeutic effect for the depression and cognitive impairment in mice. C57 BL/6J mice with depression and cognitive impairment were prepared by exposure to Escherichia coli K1. Oral gavage of NK112 significantly alleviated K1-induced anxious, depressive, and memory-impaired behaviours in the elevated plus maze, tail-suspension and Y-maze tasks, IL-1β, IL-6, and tumour necrosis factor (TNF)-α expression, and nuclear factor kappa beta (NF-κB) activation in the hippocampus, while K1-suppressed brain-derived neurotrophic factor (BDNF) expression increased. Treatment with NK112 also improved K1-induced myeloperoxidase activity, IL-6 and TNF-α expression, and NF-κB activation in the colon and reduced K1-induced Proteobacteria population in the gut microbiota. Heat-killed NK112 and its lysate supernatant, and precipitate fractions also improved anxiety/depression, cognitive impairment, and colitis in mice. In conclusion, NK112, even if heat-killed or lysed, alleviated K1 stress-induced colitis, anxiety/depression, and cognitive impairment by suppressing IL-6, TNF-α, and BDNF expression through the regulation of gut microbiota and NF-κB activation.

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