scholarly journals Yolk sac-derived Pdcd11-positive cells modulate zebrafish microglia differentiation through the NF-κB-Tgfβ1 pathway

2020 ◽  
Vol 28 (1) ◽  
pp. 170-183
Author(s):  
Ruimeng Yang ◽  
Ming Zhan ◽  
Miaomiao Guo ◽  
Hao Yuan ◽  
Yiqin Wang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Susceptibility Gene ◽  
Physiological Role ◽  
Vital Role ◽  
Yolk Sac ◽  
Cerebral White Matter ◽  
Neuron Development ◽  
Mature Brain ◽  
The Central Nervous System

AbstractMicroglia are the primary immune cells in the central nervous system, which plays a vital role in neuron development and neurodegenerative diseases. Microglial precursors in peripheral hematopoietic tissues colonize the central nervous system during early embryogenesis. However, how intrinsic and extrinsic signals integrate to regulate microglia’s differentiation remains undefined. In this study, we identified the cerebral white matter hyperintensities susceptibility gene, programmed cell death protein 11 (PDCD11), as an essential factor regulating microglia differentiation. In zebrafish, pdcd11 deficiency prevents the differentiation of the precursors to mature brain microglia. Although, the inflammatory featured macrophage brain colonization is augmented. At 22 h post fertilization, the Pdcd11-positive cells on the yolk sac are distinct from macrophages and neutrophils. Mechanistically, PDCD11 exerts its physiological role by differentially regulating the functions of nuclear factor-kappa B family members, P65 and c-Rel, suppressing P65-mediated expression of inflammatory cytokines, such as tnfα, and enhancing the c-Rel-dependent appearance of tgfβ1. The present study provides novel insights in understanding microglia differentiation during zebrafish development.

The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis

2019 ◽  
Vol 20 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Yi Wu ◽  
Hengxun He ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropeptide Y ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
Vital Role ◽  
Gut Peptides ◽  
Nonalcoholic Fatty Liver ◽  
The Central Nervous System

Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.

scholarly journals CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Peiqing Chen ◽  
Wenjuan Zhao ◽  
Yanjie Guo ◽  
Juan Xu ◽  
Ming Yin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Early Diagnosis ◽  
Vital Role ◽  
Therapeutic Interventions ◽  
Chemokine Ligand ◽  
The Central Nervous System ◽  
Receptor Cx3cr1

CX3C chemokine ligand 1 (CX3CL1) is an intriguing chemokine belonging to the CX3C family. CX3CL1 is secreted by neurons and plays an important role in modulating glial activation in the central nervous system after binding to its sole receptor CX3CR1 which mainly is expressed on microglia. Emerging data highlights the beneficial potential of CX3CL1-CX3CR1 in the pathogenesis of Alzheimer’s disease (AD), a common progressive neurodegenerative disease, and in the progression of which neuroinflammation plays a vital role. Even so, the importance of CX3CL1/CX3CR1 in AD is still controversial and needs further clarification. In this review, we make an attempt to present a concise map of CX3CL1-CX3CR1 associated with AD to find biomarkers for early diagnosis or therapeutic interventions.

scholarly journals A STRUCTURAL ANALYSIS OF THE MYELIN SHEATH IN THE CENTRAL NERVOUS SYSTEM

1967 ◽  
Vol 34 (2) ◽  
pp. 555-567 ◽  
Author(s):  
Asao Hirano ◽  
Herbert M. Dembitzer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Electron Microscope ◽  
Myelin Sheath ◽  
Cerebral White Matter ◽  
Experimental Conditions ◽  
Myelin Sheaths ◽  
Basic Theme ◽  
Cell Processes ◽  
The Central Nervous System

The cerebral white matter of rats subjected to a variety of noxious experimental conditions was examined in the electron microscope. Several unusual configurations of the myelin sheath are identified in addition to the usual configuration. These variations include the presence of (a) formed organelles within the inner and outer loops, (b) isolated islands of cytoplasm in unfused portions of the major dense lines, (c) apparently unconnected cell processes between the sheath and the axon, and (d) concentric, double myelin sheaths. A generalized model of the myelin sheath based on a hypothetical unrolling of the sheath is described. It consists of a shovel-shaped myelin sheet surrounded by a continuous thickened rim of cytoplasm. Most of the unusual myelin configurations are explained as simple variations on this basic theme. With the help of this model, an explanation of the formation of the myelin sheath is offered. This explanation involves the concept that myelin formation can occur at all cytoplasmic areas adjacent to the myelin proper and that adjacent myelin lamellae can move in relation to each other.

scholarly journals Zinc in the Brain: Friend or Foe?

2020 ◽  
Vol 21 (23) ◽  
pp. 8941
Author(s):  
Seunghyuk Choi ◽  
Dae Ki Hong ◽  
Bo Young Choi ◽  
Sang Won Suh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Metal Ion ◽  
Physiological Role ◽  
Multiple Roles ◽  
Antioxidant Function ◽  
Pathophysiological Role ◽  
The Central Nervous System ◽  
Biological Component ◽  
The Brain

Zinc is a trace metal ion in the central nervous system that plays important biological roles, such as in catalysis, structure, and regulation. It contributes to antioxidant function and the proper functioning of the immune system. In view of these characteristics of zinc, it plays an important role in neurophysiology, which leads to cell growth and cell proliferation. However, after brain disease, excessively released and accumulated zinc ions cause neurotoxic damage to postsynaptic neurons. On the other hand, zinc deficiency induces degeneration and cognitive decline disorders, such as increased neuronal death and decreased learning and memory. Given the importance of balance in this context, zinc is a biological component that plays an important physiological role in the central nervous system, but a pathophysiological role in major neurological disorders. In this review, we focus on the multiple roles of zinc in the brain.

scholarly journals The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Chaoran Chen ◽  
Xiang Zhou ◽  
Jialiang He ◽  
Zhenxing Xie ◽  
Shufang Xia ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Vital Role ◽  
Pathological Process ◽  
Peripheral Organs ◽  
Multiple Organs ◽  
Long Time ◽  
The Central Nervous System

Ischemia-reperfusion (I/R) injury is a common pathological process, which may lead to dysfunctions and failures of multiple organs. A flawless medical way of endogenous therapeutic target can illuminate accurate clinical applications. γ-Aminobutyric acid (GABA) has been known as a marker in I/R injury of the central nervous system (mainly in the brain) for a long time, and it may play a vital role in the occurrence of I/R injury. It has been observed that throughout cerebral I/R, levels, syntheses, releases, metabolisms, receptors, and transmissions of GABA undergo complex pathological variations. Scientists have investigated the GABAergic enhancers for attenuating cerebral I/R injury; however, discussions on existing problems and mechanisms of available drugs were seldom carried out so far. Therefore, this review would summarize the process of pathological variations in the GABA system under cerebral I/R injury and will cover corresponding probable issues and mechanisms in using GABA-related drugs to illuminate the concern about clinical illness for accurately preventing cerebral I/R injury. In addition, the study will summarize the increasing GABA signals that can prevent I/R injuries occurring in peripheral organs, and the roles of GABA were also discussed correspondingly.

CXCL12/CXCR4/CXCR7 Chemokine Axis in the Central Nervous System: Therapeutic Targets for Remyelination in Demyelinating Diseases

2017 ◽  
Vol 23 (6) ◽  
pp. 627-648 ◽  
Author(s):  
Tianci Chu ◽  
Lisa B. E. Shields ◽  
Yi Ping Zhang ◽  
Shi-Qing Feng ◽  
Christopher B. Shields ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vital Role ◽  
Pathological Process ◽  
Demyelinating Diseases ◽  
Myelin Repair ◽  
Chemokine Cxcl12 ◽  
The Central Nervous System ◽  
Oligodendrocyte Precursor ◽  
Oligodendrocyte Development

The chemokine CXCL12 plays a vital role in regulating the development of the central nervous system (CNS) by binding to its receptors CXCR4 and CXCR7. Recent studies reported that the CXCL12/CXCR4/CXCR7 axis regulates both embryonic and adult oligodendrocyte precursor cells (OPCs) in their proliferation, migration, and differentiation. The changes in the expression and distribution of CXCL12 and its receptors are tightly associated with the pathological process of demyelination in multiple sclerosis (MS), suggesting that modulating the CXCL12/CXCR4/CXCR7 axis may benefit myelin repair by enhancing OPC recruitment and differentiation. This review aims to integrate the current findings of the CXCL12/CXCR4/CXCR7 signaling pathway in the CNS and to highlight its role in oligodendrocyte development and demyelinating diseases. Furthermore, this review provides potential therapeutic strategies for myelin repair by analyzing the relevance between the pathological changes and the regulatory roles of CXCL12/CXCR4/CXCR7 during MS.

scholarly journals NEUROMODULATOR LIGAND-RECEPTOR SYSTEM TIP39 - PTH2R

2020 ◽  
Vol 10 (2) ◽  
pp. 78-85
Author(s):  
A. N. Kurzanov ◽  
I. M. Bykov
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Signal Transmission ◽  
Physiological Role ◽  
Receptor System ◽  
Axon Terminals ◽  
Nociceptive Information ◽  
The Central Nervous System ◽  
Anxiety Depression

Widely spread axon terminals of TIP39 neurons have a distribution similar to PTH2R containing neurons and their fibers which provides an anatomic base of neuromodulation action of TIP39. This functional and anatomic link- ing lets state that TIP39 and PTH2R form a neuromodulator ligand-receptor system. Basing on mechanisms of signal transmission used by TIP39 and PTH2R, they can form a neuromodulator system in many brain parts. TIP39-PTH2R system is a unique neuropeptide-receptor system, which localization and functions in the central nervous system differ from any other neuropeptides. Neuromodulator system TIP39-PTH2R predominantly participates in neuroendocrinal modulation by affecting the endocrinal system by means of its presence in several areas of hypothalamus. TIP39 influences neurons that contain somatostatin and corticotropin-releasing hormone. TIP39 can affect the release of adrenocorticotropin, luteinizing hormone, growth hormone and arginine-vasopressin from hypophysis. Experimental data prove that TIP39 modulates regulatory network of anxiety and depression, several aspects of stress reaction and also controls body temperature, participates in processing of auditory and nociceptive information. Physiological role of TIP39-PTH2R system is still to some extent unknown. However, distribution of PTH2R and TIP39 in tissues outside central nervous system assumes other potential physiological effects for this signal way. It is assumed that TIP39- PTH2R system should be probably considered as a potential therapeutic target for treatment of anxiety, depression and chronic pain, control and correction of neuroendocrine disruptions.

scholarly journals Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

2005 ◽  
Vol 152 (5) ◽  
pp. 791-803 ◽  
Author(s):  
Åse-Karine Fjeldheim ◽  
Per Ivar Høvring ◽  
Ole-Petter Løseth ◽  
Per Wiik Johansen ◽  
Joel C Glover ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mrna Expression ◽  
Physiological Role ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Central Nervous System ◽  
Plasma Prl

Background: The accepted function of the hypothalamic peptide, thyrotrophin-releasing hormone (TRH), is to initiate release of thyrotrophin (TSH) from the pituitary. A physiological role for TRH in lactating rats has not yet been established. Methods: Tissues were prepared from random-cycling and lactating rats and analysed using Northern blot, real time RT-PCR and quantitative in situ hybridisation. Results: This study demonstrates that TRH receptor 1 (TRHR1) mRNA expression is up-regulated in the pituitary and in discrete nuclei of the hypothalamus in lactating rats, while proTRH mRNA expression levels are increased only in the hypothalamus. The results were corroborated by quantitative in situ analysis of proTRH and TRHR1. Bromocriptine, which reduced prolactin (PRL) concentrations in plasma of lactating and nursing rats, also counteracted the suckling-induced increase in TRHR1 mRNA expression in the hypothalamus, but had an opposite effect in the pituitary. These changes were confined to the hypothalamus and the amygdala in the brain. Conclusions: The present study shows that the mechanisms of suckling-induced lactation involve region-specific regulation of TRHR1 and proTRH mRNAs in the central nervous system notably at the hypothalamic level. The results demonstrate that continued suckling is critical to maintain plasma prolactin (PRL) levels as well as proTRH and TRHR1 mRNA expression in the hypothalamus. Increased plasma PRL levels may have a positive modulatory role on the proTRH/TRHR1 system during suckling.

Sign in / Sign up

Export Citation Format

Share Document