scholarly journals Camel regulates development of the brain ventricular system

Author(s):  
Shulan Yang ◽  
Alexander Emelyanov ◽  
May-Su You ◽  
Melvin Sin ◽  
Vladimir Korzh

Abstract Development of the brain ventricular system of vertebrates and the molecular mechanisms involved are not fully understood. The developmental genes expressed in the elements of the brain ventricular system such as the ependyma and circumventricular organs act as molecular determinants of cell adhesion critical for the formation of brain ventricular system. They control brain development and function, including the flow of cerebrospinal fluid. Here, we describe the novel distantly related member of the zebrafish L1-CAM family of genes—camel. Whereas its maternal transcripts distributed uniformly, the zygotic transcripts demonstrate clearly defined expression patterns, in particular in the axial structures: floor plate, hypochord, and roof plate. camel expresses in several other cell lineages with access to the brain ventricular system, including the midbrain roof plate, subcommissural organ, organum vasculosum lamina terminalis, median eminence, paraventricular organ, flexural organ, and inter-rhombomeric boundaries. This expression pattern suggests a role of Camel in neural development. Several isoforms of Camel generated by differential splicing of exons encoding the sixth fibronectin type III domain enhance cell adhesion differentially. The antisense oligomer morpholino-mediated loss-of-function of Camel affects cell adhesion and causes hydrocephalus and scoliosis manifested via the tail curled down phenotype. The subcommissural organ’s derivative—the Reissner fiber—participates in the flow of cerebrospinal fluid. The Reissner fiber fails to form upon morpholino-mediated Camel loss-of-function. The Camel mRNA–mediated gain-of-function causes the Reissner fiber misdirection. This study revealed a link between Chl1a/Camel and Reissner fiber formation, and this supports the idea that CHL1 is one of the scoliosis factors.

1976 ◽  
Vol 51 (s3) ◽  
pp. 399s-402s ◽  
Author(s):  
P. Schelling ◽  
J. S. Hutchinson ◽  
U. Ganten ◽  
G. Sponer ◽  
D. Ganten

1. Anaesthetized, nephrectomized rats were infused intravenously with unlabelled angiotensin II (AII) or with [3H]angiotensin II (3H-labelled AII). The brain ventricular system was perfused with artificial cerebrospinal fluid. The perfusate was collected from the cisterna magna and analysed for AII by radioimmunological and biochemical methods. 2. No increase of immunoreactive AII in cerebrospinal fluid could be shown during intravenous infusion of AII. 3. During intravenous infusions of 3H-labelled AII at pressor doses small amounts of radioactivity were found in cerebrospinal fluid perfusate. 4. The radioactivity of cerebrospinal fluid outflow could not be related to AII.


Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 681 ◽  
Author(s):  
Ivan B. Filippenkov ◽  
Vasily V. Stavchansky ◽  
Alina E. Denisova ◽  
Vadim V. Yuzhakov ◽  
Larisa E. Sevan’kaeva ◽  
...  

Cerebral ischaemia is the most common cause of impaired brain function. Biologically active peptides represent potential drugs for reducing the damage that occurs after ischaemia. The synthetic melanocortin derivative, ACTH(4-7)PGP (Semax), has been used successfully in the treatment of patients with severe impairment of cerebral blood circulation. However, its molecular mechanisms of action within the brain are not yet fully understood. Previously, we used the transient middle cerebral artery occlusion (tMCAO) model to study the damaging effects of ischaemia–reperfusion on the brain transcriptome in rats. Here, using RNA-Seq analysis, we investigated the protective properties of the Semax peptide at the transcriptome level under tMCAO conditions. We have identified 394 differentially expressed genes (DEGs) (>1.5-fold change) in the brains of rats at 24 h after tMCAO treated with Semax relative to saline. Following tMCAO, we found that Semax suppressed the expression of genes related to inflammatory processes and activated the expression of genes related to neurotransmission. In contrast, ischaemia–reperfusion alone activated the expression of inflammation-related genes and suppressed the expression of neurotransmission-related genes. Therefore, the neuroprotective action of Semax may be associated with a compensation of mRNA expression patterns that are disrupted during ischaemia–reperfusion conditions.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yani Dong ◽  
Likang Lyu ◽  
Haishen Wen ◽  
Bao Shi

Long noncoding RNAs (lncRNAs) have been identified to be involved in half-smooth tongue sole (Cynoglossus semilaevis) reproduction. However, studies of their roles in reproduction have focused mainly on the ovary, and their expression patterns and potential roles in the brain and pituitary are unclear. Thus, to explore the mRNAs and lncRNAs that are closely associated with reproduction in the brain and pituitary, we collected tongue sole brain and pituitary tissues at three stages for RNA sequencing (RNA-seq), the 5,135 and 5,630 differentially expressed (DE) mRNAs and 378 and 532 DE lncRNAs were identified in the brain and pituitary, respectively. The RNA-seq results were verified by RT-qPCR. Moreover, enrichment analyses were performed to analyze the functions of DE mRNAs and lncRNAs. Interestingly, their involvement in pathways related to metabolism, signal transduction and endocrine signaling was revealed. LncRNA-target gene interaction networks were constructed based on antisense, cis and trans regulatory mechanisms. Moreover, we constructed competing endogenous RNA (ceRNA) networks. In summary, this study provides mRNA and lncRNA expression profiles in the brain and pituitary to understand the molecular mechanisms regulating tongue sole reproduction.


2021 ◽  
Author(s):  
Fei Li ◽  
Tingting Li ◽  
Jia Lin ◽  
Jing Jian ◽  
Qi Zhang ◽  
...  

Abstract Background: Multiple clinical genome-wide analysis identified that chromosome 16p13.11 is a hotspot associated with neuropsychiatric disorders such as autism, schizophrenia and epilepsy. Nodal modulator 1 (NOMO1), located on human chromosome 16p13.11, was considered as a candidate gene with neuropsychiatric disorders. However, it is unknown whether the nomo1 deficiency causes neurological abnormalities, and the molecular mechanisms and pathogenesis of the NOMO1 gene remain unclear. To study the effects of nomo1 deficiency on brain development and neuropsychiatric system, a nomo1 knockout zebrafish model was established.Methods: We developed a viable vertebrate model of nomo1 loss-of-function using CRISPR/Cas9 technology and characterized nomo1 mutant zebrafish. Phenotypic and functional studies of developing nomo1 mutant zebrafish, including morphological measurements, behavioral assays, and functional mechanistic analyses, were performed.Results: Morphological differences in the phenotype of nomo1-/- zebrafish gradually became less noticeable during development, however, the enlarged interstitial spaces in midbrain and hindbrain were detected in nomo1 mutant zebrafish. Meanwhile, the nomo1 deficiency caused the change of expression levels in neurotransmitters of γ-aminobutyrate, glutamate and serotonin. Interestingly, the nomo1 loss-of-function zebrafish model exhibited social defects and repetitive behaviors in juvenile, which represented autism-like behaviors. The transcriptome analysis showed different gene expression patterns in mutant zebrafish at the genetic level. Further results revealed that the neuroactive drug PTZ recovered the decreased locomotor phenotype in larval mutant zebrafish.Conclusions: In this study, we established a nomo1 vertebrate animal model using CRISPR/Cas9 gene editing approach. The loss-of-function of nomo1 displayed autism-like behaviors and altered levels of the γ-aminobutyrate, glutamate and serotonin in zebrafish, which provide evidence that nomo1 as a candidate gene for autism. The versatility of zebrafish model is contributed to studying NOMO1-related disorders and conducting drug screening in future.Limitations: Further studies are needed to determine whether an intervention with a neuroactive drug in nomo1-/- zebrafish to alter the behavioral phenotype is applicable to the behavior of human patients.


1965 ◽  
Vol 208 (6) ◽  
pp. 1058-1064 ◽  
Author(s):  
Leonard Graziani ◽  
Anthony Escriva ◽  
Robert Katzman

Ca exchange was measured in anesthetized cats during steady-state ventriculocisternal perfusions. When Ca45 was added to the perfusate the efflux coefficient from CSF averaged 0.025 ml/min of CSF cleared of Ca45. This coefficient was independent of CSF Ca concentration, indicating passive diffusion. About onethird of this isotope was recovered in brain tissue, two-thirds presumably diffused into blood. The brain radioactivity was localized to areas immediately adjacent to the CSF pathway. When the isotope was given systemically, the efflux coefficient into the ventricular system averaged 0.015 ml/min of serum effectively cleared of Ca45. In these experiments the specific activity of the CSF approached that of the serum. At the same time the specific activity of the brain Ca was low. Hence, the chief source of the Ca entering CSF must be blood. The rate of movement of Ca45 from blood to CSF was not altered when CSF formation was suppressed by adding acetazolamide or lowering the pH of the perfusate. This suggests that Ca transport is independent of the bulk fluid formation.


1971 ◽  
Vol 34 (3) ◽  
pp. 412-416
Author(s):  
Robert H. Wilkins ◽  
Wang-Kuen Wu

✓ Two cases are reported in which spontaneous rupture of a metastatic brain tumor occurred into the ventricular system, leading to the dissemination of the tumor contents in the cerebrospinal fluid. The site of rupture was demonstrated by ventriculography in the first case and by surgical exposure in the second. These cases support the assumption that metastatic neoplasms within the brain may rupture into the ventricular system and spread via the cerebrospinal fluid pathways.


2020 ◽  
Author(s):  
Susie S.Y. Huang ◽  
Melanie Makhlouf ◽  
Eman H. AbouMoussa ◽  
Mayra L. Ruiz Tejada Segura ◽  
Lisa S. Mathew ◽  
...  

ABSTRACTDifferent fasting regimens are known to promote health, mitigate chronic immunological disorders, and improve age-related pathophysiological parameters in animals and humans. Indeed, several clinical trials are currently ongoing using fasting as a potential therapy for a wide range of conditions. Fasting alters metabolism by acting as a reset for energy homeostasis. However, the molecular mechanisms underlying the beneficial effects of short-term fasting (STF) are still not well understood, particularly at the systems or multi-organ level. Here, we investigated the dynamic gene expression patterns associated with six periods of STF in nine different mouse organs. We cataloged the transcriptional dynamics within and between organs during STF and discovered differential temporal effects of STF among organs. Using gene ontology enrichment analysis, we identified an organ network sharing 37 common biological pathways perturbed by STF. This network incorporates the brain, liver, interscapular brown adipose tissue, and posterior-subcutaneous white adipose tissue, hence we named it the brain-liver-fats organ network. Using Reactome pathways analysis, we identified the immune system, dominated by T cell regulation processes, as a central and prominent target of systemic modulations during STF in this organ network. The changes we identified in specific immune components point to the priming of adaptive immunity and parallel the fine-tuning of innate immune signaling. Our study provides a comprehensive multi-organ transcriptomic profiling of mice subjected to multiple periods of STF, and adds new insights into the molecular modulators involved in the systemic immuno-transcriptomic changes that occur during short-term energy loss.


2020 ◽  
Vol 16 (01) ◽  
pp. 69-70
Author(s):  
DN Borakhatariya ◽  
Rupesh J Raval ◽  
Karsan B Vala ◽  
Bakti P Chavda ◽  
Sanny G Prajapati

There are several types of fetal dropsy (fetal ascites, fetal anasarca, fetal hydrocephalus), which have obstetrical importance preventing normal easy delivery of calf. Hydrocephalus is one of the fetal causes of dystocia. It is characterized by an accumulation of fluid which may be in the ventricular system or between the brain and the subarachnoid space. The swelling or enlargement of cranium occurs as a result of an imbalance between formation and drainage of cerebrospinal fluid (Arthur et al., 2001). This congenital dropsical condition is associated with an autosomal recessive gene, whereas some cases are due to BVD-MD or bluetongue virus infection in bovine (Roberts, 1986). Though this dropsical condition is rare in Gir cattle, it is reported in many other species (Dhami et al., 2007; Kumar et al., 2010; Parmar et al., 2018). The present case report depicts an unusual instance of hydrocephalic monster in an indigenous Gir calf, causing dystocia, which was successfully managed by per vaginum.


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