scholarly journals Microglia in the developing retina

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Fenge Li ◽  
Danye Jiang ◽  
Melanie A. Samuel
Keyword(s):  
Molecular Mechanisms ◽  
Neuron Development ◽  
Laminar Organization ◽  
Retina Development ◽  
Retinal Microglia ◽  
Mammalian Retina ◽  
Underlying Mechanisms ◽  
And Function ◽  
Neuron Function ◽  
The Brain

AbstractMicroglia are increasingly shown to be key players in neuron development and synapse connectivity. However, the underlying mechanisms by which microglia regulate neuron function remain poorly understood in part because such analysis is challenging in the brain where neurons and synapses are intermingled and connectivity is only beginning to be mapped. Here, we discuss the features and function of microglia in the ordered mammalian retina where the laminar organization of neurons and synapses facilitates such molecular studies. We discuss microglia origins and consider the evidence for molecularly distinct microglia subpopulations and their potential for differential roles with a particular focus on the early stages of retina development. We then review the models and methods used for the study of these cells and discuss emerging data that link retina microglia to the genesis and survival of particular retina cell subtypes. We also highlight potential roles for microglia in shaping the development and organization of the vasculature and discuss cellular and molecular mechanisms involved in this process. Such insights may help resolve the mechanisms by which retinal microglia impact visual function and help guide studies of related features in brain development and disease.

scholarly journals An Update on the Effects of Glyceollins on Human Health: Possible Anticancer Effects and Underlying Mechanisms

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 79 ◽  
Author(s):  
Thu Ha Pham ◽  
Sylvain Lecomte ◽  
Theo Efstathiou ◽  
Francois Ferriere ◽  
Farzad Pakdel
Keyword(s):  
Signaling Pathways ◽  
Human Health ◽  
Molecular Mechanisms ◽  
Biologically Active ◽  
Receptor Protein ◽  
Lipid Kinase ◽  
New Family ◽  
Anticancer Effects ◽  
Underlying Mechanisms ◽  
And Function

Biologically active plant-based compounds, commonly referred to as phytochemicals, can influence the expression and function of various receptors and transcription factors or signaling pathways that play vital roles in cellular functions and are then involved in human health and diseases. Thus, phytochemicals may have a great potential to prevent and treat chronic diseases. Glyceollins, a group of phytoalexins that are isolated from soybeans, have attracted attention because they exert numerous effects on human functions and diseases, notably anticancer effects. In this review, we have presented an update on the effects of glyceollins in relation to their potential beneficial roles in human health. Despite a growing number of studies suggesting that this new family of phytochemicals can be involved in critical cellular pathways, such as estrogen receptor, protein kinase, and lipid kinase signaling pathways, future investigations will be needed to better understand their molecular mechanisms and their specific significance in biomedical applications.

Molecular mechanisms underlying midbrain dopamine neuron development and function

2003 ◽  
Vol 480 (1-3) ◽  
pp. 75-88 ◽  
Author(s):  
Marten P. Smidt ◽  
Simone M. Smits ◽  
J.Peter H. Burbach
Keyword(s):  
Molecular Mechanisms ◽  
Dopamine Neuron ◽  
Neuron Development ◽  
Midbrain Dopamine ◽  
And Function

scholarly journals Regulation of Reelin functions by specific proteolytic processing in the brain

2021 ◽  
Author(s):  
Mitsuharu Hattori ◽  
Takao Kohno
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Migration ◽  
Molecular Mechanisms ◽  
Proteolytic Processing ◽  
Postnatal Brain ◽  
Dendrite Development ◽  
Mature Brain ◽  
Neuropsychiatric Diseases ◽  
And Function ◽  
The Brain

Abstract The secreted glycoprotein Reelin plays important roles in both brain development and function. During development, Reelin regulates neuronal migration and dendrite development. In the mature brain, the glycoprotein is involved in synaptogenesis and synaptic plasticity. It has been suggested that Reelin loss or decreased function contributes to the onset and/or deterioration of neuropsychiatric diseases, including schizophrenia and Alzheimer’s disease. While the molecular mechanisms underpinning Reelin function remain unclear, recent studies have suggested that the specific proteolytic cleavage of Reelin may play central roles in the embryonic and postnatal brain. In this review, we focus on Reelin proteolytic processing and review its potential physiological roles.

scholarly journals Mapping Meditative States and Stages with Electrophysiology: Concepts, Classifications, and Methods

2018 ◽  
Author(s):  
Poppy Schoenberg ◽  
David R Vago
Keyword(s):  
Structure And Function ◽  
Human Consciousness ◽  
Biological Structure ◽  
Contemplative Practices ◽  
States Of Consciousness ◽  
Neurobiological Substrates ◽  
Underlying Mechanisms ◽  
And Function ◽  
The Mind ◽  
The Brain

Exploration of human consciousness remains a final frontier within basic neuroscience; that is, how the finite biological structure and function of the brain gives rise to the seemingly infinite expanse that encompasses the terrain of the mind. Contemporary mindfulness and other contemplative practices across historical and post-modern traditions involve systematic forms of mental training that allow the practitioner to develop the mind in very specific and quantifiable ways. Some fundamental questions pertain to this scientific enquiry; (1) how to concisely classify discrete and developmentally-specific “mind states” of consciousness that are in line with the subtle complex phenomenology of experience so to yield ontological quantifications? (2) what measures best represent such classification/quantification systems? (3) can the present electrophysiological purview map developmentally-specified mind states and stages to neurobiological substrates, based on extant contention (i.e. discrete EEG band functionality, phenomenological significance, and underlying mechanisms) regarding the interpretation of EEG physiology?

scholarly journals Neutrophils Return to Bloodstream Through the Brain Blood Vessel After Crosstalk With Microglia During LPS-Induced Neuroinflammation

2020 ◽  
Vol 8 ◽  
Author(s):  
Yu Rim Kim ◽  
Young Min Kim ◽  
Jaeho Lee ◽  
Joohyun Park ◽  
Jong Eun Lee ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Molecular Mechanisms ◽  
Morphological Changes ◽  
Neutrophil Infiltration ◽  
Two Photon ◽  
Activated State ◽  
The Central Nervous System ◽  
Time Observation ◽  
And Function ◽  
The Brain

The circulatory neutrophil and brain tissue-resident microglia are two important immune cells involved in neuroinflammation. Since neutrophils that infiltrate through the brain vascular vessel may affect the immune function of microglia in the brain, close investigation of the interaction between these cells is important in understanding neuroinflammatory phenomena and immunological aftermaths that follow. This study aimed to observe how morphology and function of both neutrophils and microglia are converted in the inflamed brain. To directly investigate cellular responses of neutrophils and microglia, LysMGFP/+ and CX3CR1GFP/+ mice were used for the observation of neutrophils and microglia, respectively. In addition, low-dose lipopolysaccharide (LPS) was utilized to induce acute inflammation in the central nervous system (CNS) of mice. Real-time observation on mice brain undergoing neuroinflammation via two-photon intravital microscopy revealed various changes in neutrophils and microglia; namely, neutrophil infiltration and movement within the brain tissue increased, while microglia displayed morphological changes suggesting an activated state. Furthermore, neutrophils seemed to not only actively interact with microglial processes but also exhibit reverse transendothelial migration (rTEM) back to the bloodstream. Thus, it may be postulated that, through crosstalk with neutrophils, macrophages are primed to initiate a neuroinflammatory immune response; also, during pathogenic events in the brain, neutrophils that engage in rTEM may deliver proinflammatory signals to peripheral organs outside the brain. Taken together, these results both show that neuroinflammation results in significant alterations in neutrophils and microglia and lay the pavement for further studies on the molecular mechanisms behind such changes.

scholarly journals Glycosphingolipids and neuroinflammation in Parkinson’s disease

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Karim Belarbi ◽  
Elodie Cuvelier ◽  
Marie-Amandine Bonte ◽  
Mazarine Desplanque ◽  
Bernard Gressier ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Lewy Bodies ◽  
Inflammasome Activation ◽  
Nigrostriatal Pathway ◽  
Neurodegenerative Process ◽  
And Function ◽  
The Brain

Abstract Parkinson's disease is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons of the nigrostriatal pathway and the formation of neuronal inclusions known as Lewy bodies. Chronic neuroinflammation, another hallmark of the disease, is thought to play an important role in the neurodegenerative process. Glycosphingolipids are a well-defined subclass of lipids that regulate crucial aspects of the brain function and recently emerged as potent regulators of the inflammatory process. Deregulation in glycosphingolipid metabolism has been reported in Parkinson’s disease. However, the interrelationship between glycosphingolipids and neuroinflammation in Parkinson’s disease is not well known. This review provides a thorough overview of the links between glycosphingolipid metabolism and immune-mediated mechanisms involved in neuroinflammation in Parkinson’s disease. After a brief presentation of the metabolism and function of glycosphingolipids in the brain, it summarizes the evidences supporting that glycosphingolipids (i.e. glucosylceramides or specific gangliosides) are deregulated in Parkinson’s disease. Then, the implications of these deregulations for neuroinflammation, based on data from human inherited lysosomal glycosphingolipid storage disorders and gene-engineered animal studies are outlined. Finally, the key molecular mechanisms by which glycosphingolipids could control neuroinflammation in Parkinson’s disease are highlighted. These include inflammasome activation and secretion of pro-inflammatory cytokines, altered calcium homeostasis, changes in the blood-brain barrier permeability, recruitment of peripheral immune cells or production of autoantibodies.

scholarly journals Putative Role of MicroRNA-Regulated Pathways in Comorbid Neurological and Cardiovascular Disorders

2009 ◽  
Vol 2009 ◽  
pp. 1-5 ◽  
Author(s):  
Sébastien S. Hébert
Keyword(s):  
Mirna Expression ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Heart Cell ◽  
Cardiovascular Disorders ◽  
Increased Risk ◽  
Mirna Expression Profiles ◽  
And Function ◽  
The Brain

Background. The conserved noncoding microRNAs (miRNAs) that function to regulate gene expression are essential for the development and function of the brain and heart. Changes in miRNA expression profiles are associated with an increased risk for developing neurodegenerative disorders as well as heart failure. Here, the hypothesis of how miRNA-regulated pathways could contribute to comorbid neurological and cardiovascular disorders will be discussed. Presentation. Changes in miRNA expression occurring in the brain and heart could have an impact on coexisting neurological and cardiovascular characteristics by (1) modulating organ function, (2) accentuating cellular stress, and (3) impinging on neuronal and/or heart cell survival. Testing. Evaluation of miRNA expression profiles in the brain and heart tissues from individuals with comorbid neurodegenerative and cardiovascular disorders will be of great importance and relevance. Implications. Careful experimental design will shed light to the deeper understanding of the molecular mechanisms tying up those different but yet somehow connected diseases.

scholarly journals Autism: A “Critical Period” Disorder?

2011 ◽  
Vol 2011 ◽  
pp. 1-17 ◽  
Author(s):  
Jocelyn J. LeBlanc ◽  
Michela Fagiolini
Keyword(s):  
Critical Period ◽  
Molecular Mechanisms ◽  
Neurodevelopmental Disorder ◽  
Repetitive Behaviors ◽  
Postnatal Life ◽  
Critical Periods ◽  
Restricted Interests ◽  
Behavioral Impairments ◽  
And Function ◽  
The Brain

Cortical circuits in the brain are refined by experience during critical periods early in postnatal life. Critical periods are regulated by the balance of excitatory and inhibitory (E/I) neurotransmission in the brain during development. There is now increasing evidence of E/I imbalance in autism, a complex genetic neurodevelopmental disorder diagnosed by abnormal socialization, impaired communication, and repetitive behaviors or restricted interests. The underlying cause is still largely unknown and there is no fully effective treatment or cure. We propose that alteration of the expression and/or timing of critical period circuit refinement in primary sensory brain areas may significantly contribute to autistic phenotypes, including cognitive and behavioral impairments. Dissection of the cellular and molecular mechanisms governing well-established critical periods represents a powerful tool to identify new potential therapeutic targets to restore normal plasticity and function in affected neuronal circuits.

scholarly journals SULTA4A1 modulates synaptic development and function by promoting the formation of PSD-95/NMDAR complex

2019 ◽  
Author(s):  
Lorenza Culotta ◽  
Benedetta Terragni ◽  
Ersilia Vinci ◽  
Alessandro Sessa ◽  
Vania Broccoli ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Biological Function ◽  
Dendritic Morphology ◽  
Synaptic Activity ◽  
Spine Density ◽  
Neuron Development ◽  
Dendritic Spine Density ◽  
And Function ◽  
The Brain

AbstractSulfotransferase 4A1 (SULT4A1) is a cytosolic sulfotransferase, that is highly conserved across species and extensively expressed in the brain. However, the biological function of SULT4A1 is unclear. SULT4A1 has been implicated in several neuropsychiatric disorders, such as Phelan-McDermid Syndrome and schizophrenia. Here, we investigate the role of SULT4A1 within neuron development and function. Our data demonstrate that SULT4A1 modulates neuronal branching complexity and dendritic spines formation. Moreover, we show that SULT4A1, by negatively regulating the catalytic activity of Pin1 towards PSD-95, facilitates NMDAR synaptic expression and function. Finally, we demonstrate that the pharmacological inhibition of Pin1 reverses the pathological phenotypes of SULT4A1 knockdown neurons by specifically restoring dendritic spine density and rescuing NMDAR-mediated synaptic transmission. Together, these findings identify SULT4A1 as a novel player in neuron development and function by modulating dendritic morphology and synaptic activity.

scholarly journals NLRP3 maintains healthy pericytes in the brain

2019 ◽  
Author(s):  
Wenqiang Quan ◽  
Qinghua Luo ◽  
Qiqiang Tang ◽  
Tomomi Furihata ◽  
Dong Li ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Collagen Type Iv ◽  
Akt Inhibitor ◽  
Wild Type Littermate ◽  
Cerebral Microvessels ◽  
Protein Levels ◽  
Type Iv ◽  
Brain Pericytes ◽  
And Function ◽  
The Brain

Abstract Background Pericytes regulate structure and function of cerebral capillaries. Growing evidence shows that pericytes are damaged in the brain of Alzheimer’s disease (AD), which potentially contributes to AD pathogenesis. NLRP3-contained inflammasome is activated in AD brain and considered as a promising target for therapy. However, how NLRP3 affects brain pericytes is unclear. In our study, we investigated physiological function of NLRP3 in pericytes. Methods Immunohistological methods and Western blot were used to investigate pericytes and vasculature in the brains of 9-month-old NLRP3-deficient and wild-type littermate mice. Pericytes were also cultured and treated with NLRP3 inhibitor, recombinant IL-1β and AKT inhibitor. Then, proliferation, apoptosis and expression of PDGFRβ and CD13 in pericytes were analysed with biochemical methods. To investigate underlying molecular mechanisms, phosphorylation of protein kinases such as AKT, ERK and NF- k B were quantified. Results We observed that NLRP3 deficiency reduced the coverage of PDGFRβ-positive pericytes and collagen type IV-immunereactive vasculature in the brain. NLRP3 deficiency was also shown to decrease PDGFRβ and CD13 proteins in isolated cerebral microvessels. In cultured pericytes, inhibition of NLRP3 with MCC950 attenuated cell proliferation but did not induce apoptosis. NLRP3 inhibition also decreased protein levels of PDGFRβ and CD13. On the contrary, treatments with IL-1β increased protein levels of PDGFRβ and CD13 in pericytes. The alteration of PDGFRβ and CD13 protein levels was correlated with phosphorylation of AKT. Inhibition of AKT reduced PDGFRβ and CD13 in cultured pericytes. Conclusions NLRP3 might be essential to maintain healthy pericytes in the brain through activating AKT. Adverse effects on brain pericytes should be considered in the possible clinical therapies with NLRP3 inhibitors.

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