A morphogen gradient of Wnt/β-catenin signalling regulates anteroposterior neural patterning in Xenopus

Development ◽  
2001 ◽  
Vol 128 (21) ◽  
pp. 4189-4201 ◽  
Author(s):  
Clemens Kiecker ◽  
Christof Niehrs
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neural Plate ◽  
Morphogen Gradient ◽  
Neural Cells ◽  
Neural Patterning ◽  
Molecular Identity ◽  
Spemann's Organizer ◽  
Necessary And Sufficient ◽  
Dose Dependent

Anteroposterior (AP) patterning of the vertebrate neural plate is initiated during gastrulation and is regulated by Spemann’s organizer and its derivatives. The prevailing model for AP patterning predicts a caudally increasing gradient of a ‘transformer’ which posteriorizes anteriorly specified neural cells. However, the molecular identity of the transforming gradient has remained elusive. We show that in Xenopus embryos (1) dose-dependent Wnt signalling is both necessary and sufficient for AP patterning of the neuraxis, (2) Wnt/β-catenin signalling occurs in a direct and long-range fashion within the ectoderm, and (3) that there is an endogenous AP gradient of Wnt/β-catenin signalling in the presumptive neural plate of the Xenopus gastrula. Our results indicate that an activity gradient of Wnt/β-catenin signalling acts as transforming morphogen to pattern the Xenopus central nervous system.

Intracerebroventricular infusion of RU28318 blocks aldosterone-salt hypertension

1990 ◽  
Vol 258 (3) ◽  
pp. E482-E484 ◽  
Author(s):  
E. P. Gomez-Sanchez ◽  
C. M. Fort ◽  
C. E. Gomez-Sanchez
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Systolic Blood Pressure ◽  
Urine Volume ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Salt Hypertension ◽  
The Central Nervous System ◽  
Dose Dependent

The chronic intracerebroventricular (icv) infusion of aldosterone in rats and dogs elevates the blood pressure within 10-14 days at doses far below those that produce hypertension systemically. The effect in rats is dose dependent and blocked by the concomitant icv infusion of the antimineralocorticoid, prorenone. The effect of the icv infusion of RU28318, another specific spironolactone mineralocorticoid antagonist, on the hypertension produced by chronic subcutaneous (sc) administration of aldosterone in sensitized rats was reported. Miniosmotic pumps were used to deliver 1 micrograms/h aldosterone sc and 1.1 micrograms/h RU8318 icv. Over a 24-day period the indirect systolic blood pressure of the control, RU28318 icv, and aldosterone sc plus RU28318 icv groups increased from 105 to 123 mmHg and were not significantly different from each other, whereas the aldosterone sc group increased to 156 mmHg. RU28318, icv or sc, did not alter the increase in urine volume produced by aldosterone sc, and there was no significant differences in weight between the groups. This study provides evidence of the importance of the central nervous system in the pathogenesis of hypertension produced by systemic mineralocorticoid excess.

scholarly journals Differential Effects of Three CanonicalToxoplasmaStrains on Gene Expression in Human Neuroepithelial Cells

2010 ◽  
Vol 79 (3) ◽  
pp. 1363-1373 ◽  
Author(s):  
Jianchun Xiao ◽  
Lorraine Jones-Brando ◽  
C. Conover Talbot ◽  
Robert H. Yolken
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Nucleotide Metabolism ◽  
Neural Cells ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Neuroepithelial Cells ◽  
The Central Nervous System

ABSTRACTStrain type is one of the key factors suspected to play a role in determining the outcome ofToxoplasmainfection. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to representative strains ofToxoplasmaby using microarray analysis to characterize the strain-specific host cell response. The study of neural cells is of interest in light of the ability ofToxoplasmato infect the brain and to establish persistent infection within the central nervous system. We found that the extents of the expression changes varied considerably among the three strains. Neuroepithelial cells infected withToxoplasmatype I exhibited the highest level of differential gene expression, whereas type II-infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to the central nervous system, while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter the expression of a clearly defined set of genes. Moreover, Ingenuity Pathways Analysis (IPA) suggests that the three lineages differ in the ability to manipulate their host; e.g., they employ different strategies to avoid, deflect, or subvert host defense mechanisms. These observed differences may explain some of the variation in the neurobiological effects of different strains ofToxoplasmaon infected individuals.

Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System

2001 ◽  
Vol 81 (2) ◽  
pp. 871-927 ◽  
Author(s):  
Nicole Baumann ◽  
Danielle Pham-Dinh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Proteolipid Protein ◽  
Demyelinating Diseases ◽  
Neural Cells ◽  
The Central Nervous System ◽  
Experimental Demyelination ◽  
Pelizaeus Merzbacher Disease ◽  
Spontaneous Mutants ◽  
Extracellular Environment

Oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), and astrocytes constitute macroglia. This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases. One of the problems in studies of the CNS is to find components, i.e., markers, for the identification of the different cells, in intact tissues or cultures. In recent years, specific biochemical, immunological, and molecular markers have been identified. Many components specific to differentiating oligodendrocytes and to myelin are now available to aid their study. Transgenic mice and spontaneous mutants have led to a better understanding of the targets of specific dys- or demyelinating diseases. The best examples are the studies concerning the effects of the mutations affecting the most abundant protein in the central nervous myelin, the proteolipid protein, which lead to dysmyelinating diseases in animals and human (jimpy mutation and Pelizaeus-Merzbacher disease or spastic paraplegia, respectively). Oligodendrocytes, as astrocytes, are able to respond to changes in the cellular and extracellular environment, possibly in relation to a glial network. There is also a remarkable plasticity of the oligodendrocyte lineage, even in the adult with a certain potentiality for myelin repair after experimental demyelination or human diseases.

Reserpine-induced central effects: pharmacological evidence for the lack of central effects of reserpine methiodide

2005 ◽  
Vol 83 (6) ◽  
pp. 509-515 ◽  
Author(s):  
Srinivas Nammi ◽  
Krishna Murthy Boini ◽  
Sushruta Koppula ◽  
Satyanarayana Sreemantula
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Target Tissue ◽  
Central Effects ◽  
Anaesthetized Rats ◽  
The Central Nervous System ◽  
Rats And Mice ◽  
Dose Dependent ◽  
Higher Doses

Reserpine, an alkaloid from Rauwolfia serpentina, was widely used for its antihypertensive action. However, its use has been reduced because of its sedative and extra pyramidal symptoms. In the present investigation, reserpine methiodide (RMI), a quaternary analogue of reserpine, was synthesized and pharmacologically evaluated in rats and mice for its central (barbiturate hypnosis, spontaneous motor activity, body temperature, and avoidance of conditioned response) and peripheral actions (blood pressure) in comparison with reserpine. The results indicate that reserpine produced a dose-dependent depression of the central nervous system. RMI at doses equal to and double the equimolar doses of reserpine did not produce any behavioural changes compared with control animals. Nevertheless, both reserpine and RMI were found to produce dose-dependent reduction in the blood pressure of anaesthetized rats, although only at higher doses of RMI, indicating that quaternization of reserpine not only attenuated the entry of RMI into the central nervous system, but also reduced its access to the target tissue in the periphery. It is speculated that the hypotensive actions of RMI may also be due to peripheral depletion of catecholamines. Key words: resperine methiodide (RMI), reserpine, behaviour, blood pressure, mice, rats.

scholarly journals Physiology of Astroglia

2018 ◽  
Vol 98 (1) ◽  
pp. 239-389 ◽  
Author(s):  
Alexei Verkhratsky ◽  
Maiken Nedergaard
Keyword(s):  
Neural Networks ◽  
Central Nervous System ◽  
Nervous System ◽  
Neural Tissue ◽  
Membrane Transporters ◽  
Adaptive Plasticity ◽  
Neural Cells ◽  
Levels Of Organization ◽  
The Central Nervous System ◽  
Development And Aging

Astrocytes are neural cells of ectodermal, neuroepithelial origin that provide for homeostasis and defense of the central nervous system (CNS). Astrocytes are highly heterogeneous in morphological appearance; they express a multitude of receptors, channels, and membrane transporters. This complement underlies their remarkable adaptive plasticity that defines the functional maintenance of the CNS in development and aging. Astrocytes are tightly integrated into neural networks and act within the context of neural tissue; astrocytes control homeostasis of the CNS at all levels of organization from molecular to the whole organ.

scholarly journals Are astrocytes executive cells within the central nervous system?

2016 ◽  
Vol 74 (8) ◽  
pp. 671-678 ◽  
Author(s):  
Roberto E. Sica ◽  
Roberto Caccuri ◽  
Cecilia Quarracino ◽  
Francisco Capani
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Activity ◽  
Neural Cells ◽  
Degenerative Diseases ◽  
Human Species ◽  
Cerebellar Ataxias ◽  
The Central Nervous System ◽  
Experimental Findings ◽  
Lateral Sclerosis

ABSTRACT Experimental evidence suggests that astrocytes play a crucial role in the physiology of the central nervous system (CNS) by modulating synaptic activity and plasticity. Based on what is currently known we postulate that astrocytes are fundamental, along with neurons, for the information processing that takes place within the CNS. On the other hand, experimental findings and human observations signal that some of the primary degenerative diseases of the CNS, like frontotemporal dementia, Parkinson’s disease, Alzheimer’s dementia, Huntington’s dementia, primary cerebellar ataxias and amyotrophic lateral sclerosis, all of which affect the human species exclusively, may be due to astroglial dysfunction. This hypothesis is supported by observations that demonstrated that the killing of neurons by non-neural cells plays a major role in the pathogenesis of those diseases, at both their onset and their progression. Furthermore, recent findings suggest that astrocytes might be involved in the pathogenesis of some psychiatric disorders as well.

scholarly journals Widespread labeling and genomic editing of the fetal central nervous system by in utero CRISPR AAV9-PHP.eB administration

Development ◽  
2020 ◽  
Vol 148 (2) ◽  
pp. dev195586
Author(s):  
Shuntong Hu ◽  
Tao Yang ◽  
Yu Wang
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transgenic Mice ◽  
Neurodevelopmental Disorders ◽  
Genetic Manipulation ◽  
Gene Knockout ◽  
In Utero ◽  
Neural Cells ◽  
Genetic Intervention ◽  
Genomic Editing

ABSTRACTEfficient genetic manipulation in the developing central nervous system is crucial for investigating mechanisms of neurodevelopmental disorders and the development of promising therapeutics. Common approaches including transgenic mice and in utero electroporation, although powerful in many aspects, have their own limitations. In this study, we delivered vectors based on the AAV9.PHP.eB pseudo-type to the fetal mouse brain, and achieved widespread and extensive transduction of neural cells. When AAV9.PHP.eB-coding gRNA targeting PogZ or Depdc5 was delivered to Cas9 transgenic mice, widespread gene knockout was also achieved at the whole brain level. Our studies provide a useful platform for studying brain development and devising genetic intervention for severe developmental diseases.

Involvement of the 5-HT3 receptor in CRH-induced defecation in rats

1998 ◽  
Vol 274 (5) ◽  
pp. G827-G831 ◽  
Author(s):  
Keiji Miyata ◽  
Hiroyuki Ito ◽  
Shin Fukudo
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Restraint Stress ◽  
Dependent Manner ◽  
Corticotropin Releasing Hormone ◽  
Receptor Antagonists ◽  
Releasing Hormone ◽  
The Central Nervous System ◽  
Dose Dependent

We evaluated the possibility that serotonin (5-HT) mediates defecation induced by corticotropin-releasing hormone (CRH) exogenously administered or released from the central nervous system by stress via the 5-HT3 receptor in rats. Intracerebroventricular (ICV) injection of CRH (1, 3, and 10 μg/rat) dose dependently increased the number of stools excreted in rats, whereas intravenous (IV) injection of up to 100 μg/kg CRH did not affect defecation. α-Helical CRH-(9—41) and 5-HT3 receptor antagonists ramosetron and azasetron inhibited CRH (10 μg icv)-induced defecation in a dose-dependent manner with ED50 values of 4.3 μg/kg iv, 3.8 μg/kg po, and 70.4 μg/kg po, respectively. α-Helical CRH-(9—41) also inhibited CRH-induced defecation by ICV injection with an ED50 value of 0.078 μg/rat. In contrast, ramosetron and azasetron injectied ICV had no effect on CRH-induced defecation. α-Helical CRH-(9—41), ramosetron, and azasetron reduced defecation caused by restraint stress with ED50 values of 0.32, 3.6, and 19.7 μg/kg iv, respectively. These results indicate that CRH exogenously administered or released from the central nervous system by stress peripherally promotes the release of 5-HT, which in turn stimulates defecation through the 5-HT3 receptor.

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