scholarly journals Brain-Derived Neurotrophic Factor and Diabetes

2020 ◽  
Vol 21 (3) ◽  
pp. 841 ◽  
Author(s):  
Olga Rozanska ◽  
Aleksandra Uruska ◽  
Dorota Zozulinska-Ziolkiewicz
Keyword(s):  
Neurotrophic Factor ◽  
Brain Function ◽  
Clinical Problem ◽  
Brain Derived Neurotrophic Factor ◽  
Chronic Complications ◽  
Neuronal Tissue ◽  
Beneficial Impact ◽  
The Central Nervous System ◽  
And Function ◽  
Made In

Diabetes and its chronic complications still represent a great clinical problem, despite improvements made in the diagnosis and treatment of the disease. People with diabetes have a much higher risk of impaired brain function and psychiatric disorders. Neurotrophins are factors that protect neuronal tissue and improve the function of the central nervous system, and among them is brain-derived neurotrophic factor (BDNF). The level and function of BDNF in diabetes seems to be disturbed by and connected with the presence of insulin resistance. On the other hand, there is evidence for the highly beneficial impact of physical activity on brain function and BDNF level. However, it is not clear if this protective phenomenon works in the presence of diabetes. In this review, we summarize the current available research on this topic and find that the results of published studies are ambiguous.

scholarly journals A peroxisome deficiency–induced reductive cytosol state up-regulates the brain-derived neurotrophic factor pathway

2020 ◽  
Vol 295 (16) ◽  
pp. 5321-5334 ◽  
Author(s):  
Yuichi Abe ◽  
Masanori Honsho ◽  
Ryoko Kawaguchi ◽  
Takashi Matsuzaki ◽  
Yayoi Ichiki ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Neurotrophic Factor ◽  
Hippocampal Neurons ◽  
Cell Communication ◽  
Brain Derived Neurotrophic Factor ◽  
Bdnf Expression ◽  
Multiple Organs ◽  
The Central Nervous System ◽  
And Function ◽  
The Brain

The peroxisome is a subcellular organelle that functions in essential metabolic pathways, including biosynthesis of plasmalogens, fatty acid β-oxidation of very-long-chain fatty acids, and degradation of hydrogen peroxide. Peroxisome biogenesis disorders (PBDs) manifest as severe dysfunction in multiple organs, including the central nervous system (CNS), but the pathogenic mechanisms in PBDs are largely unknown. Because CNS integrity is coordinately established and maintained by neural cell interactions, we here investigated whether cell-cell communication is impaired and responsible for the neurological defects associated with PBDs. Results from a noncontact co-culture system consisting of primary hippocampal neurons with glial cells revealed that a peroxisome-deficient astrocytic cell line secretes increased levels of brain-derived neurotrophic factor (BDNF), resulting in axonal branching of the neurons. Of note, the BDNF expression in astrocytes was not affected by defects in plasmalogen biosynthesis and peroxisomal fatty acid β-oxidation in the astrocytes. Instead, we found that cytosolic reductive states caused by a mislocalized catalase in the peroxisome-deficient cells induce the elevation in BDNF secretion. Our results suggest that peroxisome deficiency dysregulates neuronal axogenesis by causing a cytosolic reductive state in astrocytes. We conclude that astrocytic peroxisomes regulate BDNF expression and thereby support neuronal integrity and function.

Development and Cell Biology of the Blood-Brain Barrier

2019 ◽  
Vol 35 (1) ◽  
pp. 591-613 ◽  
Author(s):  
Urs H. Langen ◽  
Swathi Ayloo ◽  
Chenghua Gu
Keyword(s):  
Blood Brain Barrier ◽  
Brain Function ◽  
Cell Biology ◽  
Brain Barrier ◽  
Cns Drug Delivery ◽  
Blood Brain ◽  
Barrier Formation ◽  
The Central Nervous System ◽  
Barrier Regulation ◽  
And Function

The vertebrate vasculature displays high organotypic specialization, with the structure and function of blood vessels catering to the specific needs of each tissue. A unique feature of the central nervous system (CNS) vasculature is the blood-brain barrier (BBB). The BBB regulates substance influx and efflux to maintain a homeostatic environment for proper brain function. Here, we review the development and cell biology of the BBB, focusing on the cellular and molecular regulation of barrier formation and the maintenance of the BBB through adulthood. We summarize unique features of CNS endothelial cells and highlight recent progress in and general principles of barrier regulation. Finally, we illustrate why a mechanistic understanding of the development and maintenance of the BBB could provide novel therapeutic opportunities for CNS drug delivery.

A mechanism underlying mature-onset obesity: evidence from the hyperphagic phenotype of brain-derived neurotrophic factor mutants

2004 ◽  
Vol 286 (6) ◽  
pp. R994-R1004 ◽  
Author(s):  
Edward A. Fox ◽  
Mardi S. Byerly
Keyword(s):  
Positive Feedback ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Meal Size ◽  
High Fat ◽  
Meal Pattern ◽  
Balanced Diet ◽  
High Fat Diets ◽  
The Central Nervous System ◽  
Fat Diets

Mice deficient in brain-derived neurotrophic factor (BDNF) develop mature-onset obesity, primarily due to overeating. To gain insight into the mechanism of this hyperphagia, we characterized food intake, body weight, meal pattern, and meal microstructure in young and mature mice fed balanced or high-fat diets. Hyperphagia and obesity occurred in mature but not young BDNF mutants fed a balanced diet. This hyperphagia was mediated by increased meal number, which was associated with normal meal size, meal duration, and satiety ratio. In contrast, the high-fat diet induced premature development of hyperphagia and obesity in young BDNF mutants and a similar magnitude hyperphagia in mature mutants. This hyperphagia was supported by increased meal size and was accompanied by a reduced satiety ratio. Thus the mechanism underlying hyperphagia was present before significant weight gain, but whether it occurred, and whether meal frequency or meal size was altered to support it, was modulated by a process associated with aging and by diet properties. Meal pattern changes associated with the balanced diet suggested meal initiation, and the oropharyngeal positive feedback that drives feeding, were enhanced and might have contributed to overeating in BDNF mutants, whereas negative feedback was normal. Consistent with this hypothesis, meal microstructure revealed that all hyperphagic mutant groups exhibited increased intake rates at meal onset. Therefore, the central nervous system targets of BDNF actions may include orosensory brain stem neurons that process and transmit positive feedback or forebrain neurons that modulate its strength.

scholarly journals Androgen Regulates Brain-Derived Neurotrophic Factor in Spinal Motoneurons and Their Target Musculature

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 253-261 ◽  
Author(s):  
Tom Verhovshek ◽  
Yi Cai ◽  
Mark C. Osborne ◽  
Dale R. Sengelaub
Keyword(s):  
Neurotrophic Factor ◽  
Vastus Lateralis ◽  
Brain Derived Neurotrophic Factor ◽  
Neural System ◽  
Dendritic Morphology ◽  
Trophic Factors ◽  
Interactive Effects ◽  
Neuromuscular System ◽  
Spinal Motoneurons ◽  
And Function

Abstract Trophic factors maintain motoneuron morphology and function in adulthood. Brain-derived neurotrophic factor (BDNF) interacts with testosterone to maintain dendritic morphology of spinal motoneurons. In addition, testosterone regulates BDNF’s receptor (trkB) in motoneurons innervating the quadriceps muscles as well as in motoneurons of the highly androgen-sensitive spinal nucleus of the bulbocavernosus (SNB). Given these interactive effects, we examined whether androgen might also regulate BDNF in quadriceps and SNB motoneurons and their corresponding target musculature. In both motoneuron populations, castration of males reduced BDNF immunolabeling, and this effect was prevented with testosterone replacement. ELISA for BDNF in the target musculature of quadriceps (vastus lateralis, VL) and SNB (bulbocavernosus, BC) motoneurons revealed that BDNF in the VL and BC muscles was also regulated by androgen. However, although castration significantly decreased BDNF concentration in the VL muscle, BDNF concentration in the BC muscle was significantly increased in castrates. Treatment of castrated males with testosterone maintained BDNF levels at those of intact males in both sets of muscles. Together, these results demonstrate that androgens regulate BDNF in both a sexually dimorphic, highly androgen-sensitive neuromuscular system as well as a more typical somatic neuromuscular system. Furthermore, in addition to the regulation of trkB, these studies provide another possible mechanism for the interactive effects of testosterone and BDNF on motoneuron morphology. More importantly, by examining both the motoneurons and the muscles they innervate, these results demonstrate that within a neural system, BDNF levels in different components are differentially affected by androgen manipulation.

scholarly journals Brain-Derived Neurotrophic Factor, Depression, and Physical Activity: Making the Neuroplastic Connection

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Cristy Phillips
Keyword(s):  
Physical Activity ◽  
Neurotrophic Factor ◽  
Recovery Of Function ◽  
Brain Derived Neurotrophic Factor ◽  
Brain Regions ◽  
Bdnf Level ◽  
Major Depressive ◽  
Brain Circuits ◽  
Therapeutic Mechanisms ◽  
And Function

Brain-derived neurotrophic factor (BDNF) is a neurotrophin that is vital to the survival, growth, and maintenance of neurons in key brain circuits involved in emotional and cognitive function. Convergent evidence indicates that neuroplastic mechanisms involving BDNF are deleteriously altered in major depressive disorder (MDD) and animal models of stress. Herein, clinical and preclinical evidence provided that stress-induced depressive pathology contributes to altered BDNF level and function in persons with MDD and, thereby, disruptions in neuroplasticity at the regional and circuit level. Conversely, effective therapeutics that mitigate depressive-related symptoms (e.g., antidepressants and physical activity) optimize BDNF in key brain regions, promote neuronal health and recovery of function in MDD-related circuits, and enhance pharmacotherapeutic response. A greater knowledge of the interrelationship between BDNF, depression, therapeutic mechanisms of action, and neuroplasticity is important as it necessarily precedes the derivation and deployment of more efficacious treatments.

scholarly journals A developmental stage- and Kidins220-dependent switch in astrocyte responsiveness to brain-derived neurotrophic factor

2021 ◽  
Author(s):  
Fanny Jaudon ◽  
Martina Albini ◽  
Stefano Ferroni ◽  
Fabio Benfenati ◽  
Fabrizia Cesca
Keyword(s):  
Nervous System ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Embryonic Cells ◽  
Inwardly Rectifying Potassium Channel ◽  
Complex Functions ◽  
The Central Nervous System ◽  
Homeostatic Function ◽  
Neurotrophin Signaling ◽  
Neuronal Physiology

Astroglial cells are key to maintain nervous system homeostasis. Neurotrophins are known for their pleiotropic effects on neuronal physiology, but also exert complex functions onto glial cells. In this work, we investigated: (i) the signaling competence of embryonic and postnatal primary cortical astrocytes exposed to brain-derived neurotrophic factor (BDNF); and (ii) the role of Kinase D interacting substrate (Kidins220), a transmembrane scaffold protein that mediates neurotrophin signaling in neurons, in the astrocyte response to BDNF. We found a shift from a kinase-based response in embryonic cells to a predominantly [Ca2+]i-based response in postnatal cultures associated with the decreased expression of the full-length BDNF receptor TrkB, with a contribution of Kidins220 to the BDNF-activated kinase and [Ca2+]i pathways. Finally, Kidins220 participates in astrocytes’ homeostatic function by controlling the expression of the inwardly rectifying potassium channel (Kir) 4.1 and the metabolic balance of embryonic astrocytes. Overall, our data contribute to the understanding of the complex role played by astrocytes within the central nervous system and identify Kidins220 as a novel actor in the increasing number of pathologies characterized by astrocytic dysfunctions.

Glucocorticoids change the transcript levels of galanin, galanin receptor-2 and brain-derived neurotrophic factor in rat hippocampal neurons

2018 ◽  
Author(s):  
Fangyan Pan ◽  
Chengying Yang ◽  
Qing Xie ◽  
Yang Yang ◽  
Xianmei Luo ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Hippocampal Neurons ◽  
Brain Derived Neurotrophic Factor ◽  
Control Group ◽  
High Concentration ◽  
Galanin Receptor ◽  
Mda Content ◽  
And Function ◽  
Hippocampal Structure ◽  
Transcription Expression

Glucocorticoids (GCs) can affect hippocampal structure and function in animals and humans. This study was designed to investigate the possible functional molecules and mechanisms involved in the action of GCs on hippocampal neurons. Rat primary hippocampal neurons were cultured and treated with glucocorticoids at a low concentration (LC, 10-8 mol/L), a middle concentration (MC, 10-7 mol/L) and a high concentration (HC, 10-6 mol/L). The results indicate that GCs do not change the viability of hippocampal neurons but do change the catalase (CAT) activity and malondialdehyde (MDA) content. The transcription expression levels of brain derived neurotrophic factor (BDNF), galanin (GAL), galanin receptor-2 (GALR2), and neuropeptide Y receptor-5 (NPYR5) genes in the HC group were significantly higher than those in the control group (p less than 0.05). These results suggest that hippocampal neurons launch the neuron protection pathways mediated by GAL, GALR2 and BDNF molecules when encountering an experimentally high concentration of corticosteroids.

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