Mouse fetal trisomy 13 and hypotrophy of the spinal cord: effect on calbindin-D28k and calretinin expressed by neurons of the spinal cord and dorsal root ganglia.

Details

Serval ID
serval:BIB_CA1F8A912C1A
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Mouse fetal trisomy 13 and hypotrophy of the spinal cord: effect on calbindin-D28k and calretinin expressed by neurons of the spinal cord and dorsal root ganglia.
Journal
Neuroscience
Author(s)
Ninomiya T., Vuillemin M., Walter-Barakat I., Winking H., Pexieder T., Droz B.
ISSN
0306-4522
Publication state
Published
Issued date
1993
Peer-reviewed
Oui
Volume
57
Number
4
Pages
1109-1120
Language
english
Abstract
Trisomy 13 was detected in 10% of mouse embryos obtained from pregnant females which were doubly heterozygous for Robertsonian chromosomes involving chromosome 13. The developing dorsal root ganglia and spinal cords were examined in trisomy 13 and littermate control mice between days 12 and 18 of gestation (E12-18). The overall size of the dorsal root ganglia and number of ganglion cells within a given ganglion were not altered, but the number of neurons immunoreactive for calbindin and calretinin was reduced. The trisomic spinal cord was reduced in size with neurons lying in a tightly compact distribution in the gray matter. In trisomic fetuses, the extent of the neuropil of the spinal cord was reduced, and may represent a diminished field of interneuronal connectivity, due to reduced arborization of dendritic processes of the neurons present, particularly of calbindin-immunostained neurons. Furthermore, the subpopulation of calretinin-immunoreactive neurons and axons was also reduced in developing trisomic gray and white matter, respectively. Thus, overexpression of genes on mouse chromosome 13 exerts a deleterious effect on the development of neuropil, affecting both dendritic and axonal arborization in the trisomy 13 mouse. The defect of calbindin or calretinin expression by subsets of dorsal root ganglion or spinal cord neurons may result from deficient cell-to-cell interactions with targets which are hypoplastic.
Keywords
Animals, Calcium-Binding Protein, Vitamin D-Dependent, Embryo, Mammalian, Embryonic and Fetal Development, Female, Ganglia, Spinal, Humans, Immunohistochemistry, Mice, Molecular Weight, Nerve Tissue Proteins, Neurons, Neurons, Afferent, Spinal Cord, Trisomy
Pubmed
Web of science
Create date
30/03/2009 9:14
Last modification date
20/08/2019 15:45
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