Differential expression of Hox 3.1 protein in subregions of the embryonic and adult spinal cord

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 411-420 ◽  
Author(s):  
A. Awgulewitsch ◽  
D. Jacobs
Keyword(s):  
Spinal Cord ◽  
Expression Patterns ◽  
Neuronal Cells ◽  
Distinct Pattern ◽  
Embryonic Cells ◽  
Protein Coding ◽  
Adult Mice ◽  
Adult Spinal Cord ◽  
Immunohistochemical Studies ◽  
Developing Spinal Cord

Synthetic oligopeptides derived from the predicted Hox 3.1 protein coding sequence were used for the production of antibodies (anti-aa2) that specifically recognize Hox 3.1 protein in tissue sections. These antibodies were applied in immunohistochemical studies to monitor the expression of Hox 3.1 protein within the central nervous system (CNS) of embryonic and adult mice. We demonstrate congruency between the distinct Hox 3.1 RNA and protein expression patterns in the developing spinal cord by direct comparison of in situ hybridization and immunohistochemical staining in frozen sagittal sections from embryos of 12.5 days of gestation. A distinct pattern of spatially restricted expression of Hox 3.1 protein within the spinal cord was first detected at around 10.5 days of embryonic development. Within certain anteroposterior limits the geometries of this expression pattern change drastically during subsequent embryonic stages, concomitant with important cytoarchitectural changes in the developing spinal cord. Analyses on subcellular levels indicate predominant accumulation of Hox 3.1 protein within nuclei of neuronal cells. In addition to the nuclear localization in subsets of embryonic cells, persistent accumulation of Hox 3.1 protein was shown in nuclei of fully differentiated and mature neuronal cells of the adult CNS.

scholarly journals Multiple steps mediate ventricular layer attrition to form the adult mouse spinal cord central canal

2019 ◽  
Author(s):  
Marco A. Cañizares ◽  
Aida Rodrigo Albors ◽  
Gail Singer ◽  
Nicolle Suttie ◽  
Metka Gorkic ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Proliferation ◽  
Expression Patterns ◽  
Central Canal ◽  
Floor Plate ◽  
Cell Potential ◽  
Proliferation Markers ◽  
Tissue Organization ◽  
Stem Cell Potential ◽  
Adult Spinal Cord

AbstractThe ventricular layer of the spinal cord is remodelled during embryonic development and ultimately forms the adult central canal, which retains neural stem cell potential. This anatomical transformation involves the process of dorsal collapse, however, accompanying changes in tissue organization and cell behaviour as well as the origin of cells contributing to the adult central canal are not well understood. Here we describe sequential localised cell rearrangements which contribute to the gradual attrition of the spinal cord ventricular layer during development. This includes local breakdown of the pseudostratified organisation of the dorsal ventricular layer prefiguring dorsal collapse and evidence for a new phenomenon, ventral dissociation, during which the ventral-most floor plate cells separate from a subset that are retained in the central canal. Using cell proliferation markers and cell-cycle reporter mice, we further show that following dorsal collapse, ventricular layer attrition involves an overall reduction in cell proliferation, characterised by an intriguing increase in the percentage of cells in G1/S. In contrast, programmed cell death does not contribute to ventricular layer remodelling. By analysing transcript and protein expression patterns associated with key signalling pathways, we provide evidence for a gradual decline in ventral sonic hedgehog activity and an accompanying ventral expansion of initial dorsal bone morphogenetic protein signalling, which comes to dominate the forming central canal. This study identifies multiple steps that contribute to spinal cord ventricular layer attrition and adds to increasing evidence for the heterogenous origin of the adult spinal cord central canal, which includes cells from the floor plate and the roof plate as well as ventral progenitor domain.

Open brain, a new mouse mutant with severe neural tube defects, shows altered gene expression patterns in the developing spinal cord

Development ◽  
1994 ◽  
Vol 120 (11) ◽  
pp. 3119-3130 ◽  
Author(s):  
T. Gunther ◽  
M. Struwe ◽  
A. Aguzzi ◽  
K. Schughart
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Dorsal Root Ganglia ◽  
Neural Tube ◽  
Dorsal Root ◽  
Expression Patterns ◽  
Axial Skeleton ◽  
Neural Tube Closure ◽  
Primary Defect ◽  
Developing Spinal Cord

We describe a new mouse mutation, designated open brain (opb), which results in severe defects in the developing neural tube. Homozygous opb embryos exhibited an exencephalic malformation involving the forebrain, midbrain and hindbrain regions. The primary defect of the exencephaly could be traced back to a failure to initiate neural tube closure at the midbrain-forebrain boundary. Severe malformations in the spinal cord and dorsal root ganglia were observed in the thoracic region. The spinal cord of opb mutant embryos exhibited an abnormal circular to oval shape and showed defects in both ventral and dorsal regions. In severely affected spinal cord regions, a dorsalmost region of cells negative for Wnt-3a, Msx-2, Pax-3 and Pax-6 gene expression was detected and dorsal expression of Pax-6 was increased. In ventral regions, the area of Shh and HNF-3 beta expression was enlarged and the future motor neuron horns appeared to be reduced in size. These observations indicate that opb embryos exhibit defects in the specification of cells along the dorsoventral axis of the developing spinal cord. Although small dorsal root ganglia were formed in opb mutants, their metameric organization was lost. In addition, defects in eye development and malformations in the axial skeleton and developing limbs were observed. The implications of these findings are discussed in the context of dorsoventral patterning of the developing neural tube and compared with known mouse mutants exhibiting similar defects.

scholarly journals Immunocytochemical localization of carbonic anhydrase in the spinal cords of normal and mutant (shiverer) adult mice with comparisons among fixation methods.

1985 ◽  
Vol 33 (1) ◽  
pp. 45-54 ◽  
Author(s):  
W Cammer ◽  
R Sacchi ◽  
V Sapirstein
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Carbonic Anhydrase ◽  
Immunocytochemical Staining ◽  
Immunocytochemical Localization ◽  
Paraffin Embedding ◽  
Myelinated Fibers ◽  
Adult Mice ◽  
Fibrous Astrocytes ◽  
Adult Spinal Cord

The peroxidase-antiperoxidase technique was used for immunocytochemical localization of carbonic anhydrase in the mouse spinal cord to detect whether this antigen was normally present in myelinated fibers, in oligodendrocytes in both white and gray matter, and in astrocytes, and to determine where the carbonic anhydrase might be localized in the spinal cords of dysmyelinating mutant (shiverer) mice. The most favorable methods for treating tissue were: 1) immersion in formalin-ethanol-acetic acid followed by paraffin embedding, or 2) light fixation with paraformaldehyde and preparation of vibratome sections. Carnoy's solution, followed by paraffin embedding, extracted myelin from the tissue, while aqueous aldehydes, when used before paraffin embedding, reduced staining everywhere except at sites of compact myelin. The latter conclusion was based, in part, on the almost complete loss of this antigen from the shiverer cord, where compact myelin is known to be virtually absent but where membrane-bound carbonic anhydrase was demonstrated enzymatically. When the optimal methods were used with normal mouse cords, carbonic anhydrase was found throughout the white matter columns and in the oligodendrocytes in gray and white matter. The staining of the white matter was attributed to myelinated fibers because of the similarity in distribution to both a histological myelin stain and the immunocytochemical staining for myelin basic protein. In the mutant mice the oligodendrocyte cell bodies and processes, which were stained in all areas of the spinal cord, were particularly numerous at the periphery of the sections. In contrast to the oligodendrocytes, the fibrous astrocytes appeared to lack carbonic anhydrase, or to have lower than detectable levels, since the astrocyte marker, glial fibrillary acidic protein, had a very different distribution from that of carbonic anhydrase. Even finer localization was obtained in vibratome sections, where the antibody against carbonic anhydrase permitted visualization of the processes connecting oligodendrocytes to myelinated fibers in the normal adult spinal cord.

Expression patterns of erythropoietin and its receptor in the developing spinal cord and dorsal root ganglia

2005 ◽  
Vol 210 (3) ◽  
pp. 209-219 ◽  
Author(s):  
Wolfgang Knabe ◽  
Anna-Leena Sirén ◽  
Hannelore Ehrenreich ◽  
Hans-Jürg Kuhn
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Expression Patterns ◽  
Developing Spinal Cord

Atypical pilocytic astrocytoma of adult spinal cord: A case report

2018 ◽  
pp. 1-2
Keyword(s):  
Spinal Cord ◽  
Young Adults ◽  
Case Report ◽  
Pilocytic Astrocytoma ◽  
Treatment Protocol ◽  
Pilomyxoid Astrocytoma ◽  
Standardized Treatment ◽  
Children And Young Adults ◽  
Adult Spinal Cord

Pilomyxoid astrocytoma (PMA) is an atypical subtype of pilocytic astrocytoma (PA), which presents in children and young adults. The incidence of PMA is low, so there is no standardized treatment protocol for it. Here, we present a 62-year-old woman with recurrent PMA, which is important for the understanding and treatment of the disease.

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