scholarly journals Teratological changes in postembryos of Eratigena atrica obtained by the application of alternating temperatures on spider embryos

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11457
Author(s):  
Teresa Napiórkowska ◽  
Julita Templin ◽  
Paweł Napiórkowski

Spider embryonic development depends on several factors, including temperature. Under optimum thermal conditions embryogenesis proceeds undisturbed and embryo mortality is low. On the other hand, dramatic shifts in incubation temperature may cause a range of developmental defects in embryos. It has been confirmed in numerous laboratory experiments that abrupt temperature changes can be a powerful teratogenic factor. Changes in the external structure are frequently reflected in the internal anatomy, and above all, in the central nervous system. In the present teratological study, by exposing spider embryos to the temperatures of 14 °C and 32 °C, changed every 12 hours for the first 10 days of their development, we obtained 74 postembryos of Eratigena atrica with body deformities such as oligomely, heterosymely, schistomely, bicephaly, complex anomalies and others. We selected six spiders to describe and analyze their morphological changes. In one case, that of a spider affected by polymely (the presence of a supernumerary appendage) combined with heterosymely (the fusion of walking legs), we also focused on the structure of the central nervous system. The analysis indicated that this complex anomaly was accompanied by only one change in the central nervous system: the presence of a supernumerary neuropil. Since no fusion of walking leg neuropils was observed, it was concluded that, in this instance, there was no relationship between the fusion of legs and the structure of the central nervous system.

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2340
Author(s):  
Hannah E. Henson ◽  
Michael R. Taylor

The spliceosome consists of accessory proteins and small nuclear ribonucleoproteins (snRNPs) that remove introns from RNA. As splicing defects are associated with degenerative conditions, a better understanding of spliceosome formation and function is essential. We provide insight into the role of a spliceosome protein U4/U6.U5 tri-snRNP-associated protein 1, or Squamous cell carcinoma antigen recognized by T-cells (Sart1). Sart1 recruits the U4.U6/U5 tri-snRNP complex to nuclear RNA. The complex then associates with U1 and U2 snRNPs to form the spliceosome. A forward genetic screen identifying defects in choroid plexus development and whole-exome sequencing (WES) identified a point mutation in exon 12 of sart1 in Danio rerio (zebrafish). This mutation caused an up-regulation of sart1. Using RNA-Seq analysis, we identified additional upregulated genes, including those involved in apoptosis. We also observed increased activated caspase 3 in the brain and eye and down-regulation of vision-related genes. Although splicing occurs in numerous cells types, sart1 expression in zebrafish was restricted to the brain. By identifying sart1 expression in the brain and cell death within the central nervous system (CNS), we provide additional insights into the role of sart1 in specific tissues. We also characterized sart1’s involvement in cell death and vision-related pathways.


2010 ◽  
Vol 31 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Bing Zhou ◽  
Yi-Bing Zhu ◽  
Lin Lin ◽  
Qian Cai ◽  
Zu-Hang Sheng

The autophagy–lysosomal pathway is an intracellular degradation process essential for maintaining neuronal homoeostasis. Defects in this pathway have been directly linked to a growing number of neurodegenerative disorders. We recently revealed that Snapin plays a critical role in co-ordinating dynein-driven retrograde transport and late endosomal–lysosomal trafficking, thus maintaining efficient autophagy–lysosomal function. Deleting snapin in neurons impairs lysosomal proteolysis and reduces the clearance of autolysosomes. The role of the autophagy–lysosomal system in neuronal development is, however, largely uncharacterized. Here, we report that snapin deficiency leads to developmental defects in the central nervous system. Embryonic snapin−/− mouse brain showed reduced cortical plates and intermediate zone cell density, increased apoptotic death in the cortex and third ventricle, enhanced membrane-bound LC3-II staining associated with autophagic vacuoles and an accumulation of polyubiquitinated proteins in the cortex and hippocampus. Thus our results provide in vivo evidence for the essential role of late endocytic transport and autophagy–lysosomal function in maintaining neuronal survival and development of the mammalian central nervous system. In addition, our study supports the existence of a functional interplay between the autophagy–lysosome and ubiquitin–proteasome systems in the protein quality-control process.


Author(s):  
К. Ляхова ◽  
K. Lyakhova ◽  
И. Колесникова ◽  
I. Kolesnikova ◽  
Д. Утина ◽  
...  

Purpose: Investigation of the dose–time–effect dependency of the behavior of mice and rats after irradiation with accelerated protons and comparison of these data with the morphological changes in the hippocampus and the cerebellum of rodents. Material and methods: Experiments were performed on outbred adult female ICR mice (CD-1), SPF categories, body weight 30–35 g, of the age of 10 weeks – total number 61 animals, and on 39 male Sprague Dawley outbred rats weighing 190–230 g, aged 6.5–7.5 weeks. The animals were irradiated with accelerated protons with energy of 70 MeV on the medical beam of the phasotron of the Joint Institute for Nuclear Research (Dubna). Mice were placed in individual containers and irradiated 4 ones at a time. Irradiation was performed in a modified Bragg peak at doses of 0.5; 1; 2.5 and 5 Gy in caudocranial and craniocaudal direction. Rats were divided into 2 groups: intact control and group irradiated with 170 MeV protons at a dose of 1 Gy, dose rate of 1 Gy / min in the craniocaudal direction. The behavioral responses of experimental animals were tested in the Open Field test on days 1, 7, 14, 30, 90 in rats and on days 8, 30, and 90 in mice. Quantitative analysis of the dilution of Purkinje cells in the rat cerebellum was made, as well as morphological changes in the rat hippocampal neurons. It was shown a development of structural changes after irradiation with protons in neurons of different severity at different times after exposure: after 30 and 90 days. Results: In the period of 1–8 days after proton irradiation of mice and rats in non-lethal doses (0.5–5.0 Gy), there is a dose-independent decrease in the main indicators of the spontaneous locomotor activity of rodents. By the 90th day after irradiation, there is a clear tendency to normalize the indicators of OIR in all groups of irradiated animals, while the ES remains elevated. Disruption of motor activity of rodents irradiated with protons in the early period and its relative normalization in the late post-irradiation period occur on the background of an increased number of morphologically altered and dystrophic neurons in the hippocampus and rarefied of Purkinje cells in the cerebellum. Conclusion: The complex hierarchical structure of the central nervous system, the dependence of its function on the state of the whole organism and its hormonal background, as well as on the state of the blood supply and other factors, along with its high plasticity, require complex physiological, morphological and neurochemical approaches in analyzing the radiobiological effect of corpuscular radiation, taking into consideration the unevenness in dose distribution during irradiation.


1997 ◽  
Vol 10 (4) ◽  
pp. 423-430 ◽  
Author(s):  
L. Manfrè ◽  
A. Banco ◽  
M. Accardi ◽  
V. D'Antonio ◽  
A. Caronia ◽  
...  

As for all the central nervous system (CNS) defects, the severity of eye malformations is related to the time a teratogenic factor occurs: the earlier the insult, the more serious the eye abnormalities are. Magnetic resonance imaging perfectly depicts most eye defects. Considering that several CNS malformations have been described to occur simultaneously in the case of eye abnormalities, MRI is considered the imaging modality of choice nowadays.


2012 ◽  
Vol 50 (1) ◽  
pp. 122-143 ◽  
Author(s):  
P. Wohlsein ◽  
U. Deschl ◽  
W. Baumgärtner

In the central nervous system (CNS) of domestic animals, numerous specialized normal structures, unusual cell types, findings of uncertain or no significance, artifacts, and various postmortem alterations can be observed. They may cause confusion for inexperienced pathologists and those not specialized in neuropathology, leading to misinterpretations and wrong diagnoses. Alternatively, changes may mask underlying neuropathological processes. “Specialized structures” comprising the hippocampus and the circumventricular organs, including the vascular organ of the lamina terminalis, subfornical organ, subcommissural organ, pineal gland, median eminence/neurohypophyseal complex, choroid plexus, and area postrema, are displayed. Unusual cell types, including cerebellar external germinal cells, CNS progenitor cells, and Kolmer cells, are presented. In addition, some newly recognized cell types as of yet incompletely understood significance and functionality, such as synantocytes and aldynoglia, are introduced and described. Unusual reactive astrocytes in cats, central chromatolysis, neuronal vacuolation, spheroids, spongiosis, satellitosis, melanosis, neuromelanin, lipofuscin, polyglucosan bodies, and psammoma bodies may represent incidental findings of uncertain or no significance and should not be confused with significant microscopic changes. Auto- and heterolysis as well as handling and histotechnological processing may cause postmortem morphological changes of the CNS, including vacuolization, cerebellar conglutination, dark neurons, Buscaino bodies, freezing, and shrinkage artifacts, all of which have to be differentiated from genuine lesions. Postmortem invasion of micro-organisms should not be confused with intravital infections. Awareness of these different changes and their recognition are a prerequisite for identifying genuine lesions and may help to formulate a professional morphological and etiological diagnosis.


1980 ◽  
Vol 61 (4) ◽  
pp. 42-46
Author(s):  
H. M. Shulman ◽  
N. P. Popov

The clinical picture of the lesion and the results of a morphological study of a patient with osteochondrosis of the lumbar spine with compression of the spinal roots are described. Morphological changes of a degenerative-dystrophic nature were found not only in the formations located in the compression focus, but also in the peripheral neuromuscular apparatus, segmental and suprasegmental structures of the central nervous system.


Sign in / Sign up

Export Citation Format

Share Document