scholarly journals Isolation of a Mouse Motoneuron-Enriched Fraction from Mouse Spinal Cord on a Density Barrier

2002 ◽  
Vol 2 ◽  
pp. 1544-1546 ◽  
Author(s):  
John Graham
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Tissue ◽  
Low Density ◽  
Mouse Spinal Cord ◽  
Mechanical Disruption ◽  
Density Barrier

After a combined enzymic and mechanical disruption of the spinal cord tissue, the low-density motoneurons band at the interface of a 1.06-g/ml barrier through which other contaminating cells sediment.

scholarly journals Interpreting the biochemical specificity of mouse spinal cord by confocal raman microspectral imaging

2017 ◽  
Vol 10 (05) ◽  
pp. 1743007 ◽  
Author(s):  
Yuze Gong ◽  
Zhuowen Liang ◽  
Yaning Yin ◽  
Jiwei Song ◽  
Xueyu Hu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ex Vivo ◽  
Distribution Patterns ◽  
Chemical Components ◽  
Spinal Cord Tissue ◽  
Essential Requirement ◽  
Mouse Spinal Cord ◽  
Molecular Investigation ◽  
Specific Substance ◽  
Biochemical Mechanisms

Interpreting the biochemical specificity of spinal cord tissue is the essential requirement for understanding the biochemical mechanisms during spinal-cord-related pathological course. In this work, a longitudinal study was implemented to reveal a precise linkage between the spectral features and the molecular composition in ex vivo mouse spinal cord tissue by microspectral Raman imaging. It was testified that lipid-rich white matter could be distinguished from gray matter not only by the lipid Raman peaks at 1064, 1300, 1445 and 1660[Formula: see text]cm[Formula: see text], but also by protein (1250 and 1328[Formula: see text]cm[Formula: see text] and saccharides (913 and 1137[Formula: see text]cm[Formula: see text] distributions. [Formula: see text]-means cluster analysis was further applied to visualize the morphological basis of spinal cord tissue by chemical components and their distribution patterns. Two-dimensional chemical images were then generated to visualize the contrast between two different tissue types by integrating the intensities of the featured Raman bands. All the obtained results illustrated the biochemical characteristics of spinal cord tissue, as well as some specific substance variances between different tissue types, which formed a solid basis for the molecular investigation of spinal cord pathological alterations.

Antisera to different glycolipids induce myelin alterations in mouse spinal cord tissue cultures

1985 ◽  
Vol 339 (1) ◽  
pp. 9-18 ◽  
Author(s):  
German A. Roth ◽  
Matias Röyttä ◽  
Robert K. Yu ◽  
Cedric S. Raine ◽  
Murray B. Bornstein
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Tissue ◽  
Tissue Cultures ◽  
Mouse Spinal Cord

scholarly journals Basal Lamina Formation by Astrocytes in Organotypic Cultures of Mouse Spinal Cord Tissue

1985 ◽  
Vol 44 (3) ◽  
pp. 295-303 ◽  
Author(s):  
HIROFUMI KUSAKA ◽  
ASAO HlRANO ◽  
Murray B. Bornstein ◽  
Cedric S. Raine
Keyword(s):  
Spinal Cord ◽  
Basal Lamina ◽  
Spinal Cord Tissue ◽  
Organotypic Cultures ◽  
Mouse Spinal Cord

scholarly journals Enhanced Function and Overexpression of Metabotropic Glutamate Receptors 1 and 5 in the Spinal Cord of the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis during Disease Progression

2019 ◽  
Vol 20 (18) ◽  
pp. 4552 ◽  
Author(s):  
Tiziana Bonifacino ◽  
Claudia Rebosio ◽  
Francesca Provenzano ◽  
Carola Torazza ◽  
Matilde Balbi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Amyotrophic Lateral Sclerosis ◽  
Metabotropic Glutamate Receptors ◽  
Disease Stage ◽  
Spinal Cord Tissue ◽  
Mouse Spinal Cord ◽  
Sod1g93a Mice ◽  
Group I ◽  
Sod1g93a Mouse ◽  
Lateral Sclerosis

Glutamate (Glu)-mediated excitotoxicity is a major cause of amyotrophic lateral sclerosis (ALS) and our previous work highlighted that abnormal Glu release may represent a leading mechanism for excessive synaptic Glu. We demonstrated that group I metabotropic Glu receptors (mGluR1, mGluR5) produced abnormal Glu release in SOD1G93A mouse spinal cord at a late disease stage (120 days). Here, we studied this phenomenon in pre-symptomatic (30 and 60 days) and early-symptomatic (90 days) SOD1G93A mice. The mGluR1/5 agonist (S)-3,5-Dihydroxyphenylglycine (3,5-DHPG) concentration dependently stimulated the release of [3H]d-Aspartate ([3H]d-Asp), which was comparable in 30- and 60-day-old wild type mice and SOD1G93A mice. At variance, [3H]d-Asp release was significantly augmented in 90-day-old SOD1G93A mice and both mGluR1 and mGluR5 were involved. The 3,5-DHPG-induced [3H]d-Asp release was exocytotic, being of vesicular origin and mediated by intra-terminal Ca2+ release. mGluR1 and mGluR5 expression was increased in Glu spinal cord axon terminals of 90-day-old SOD1G93A mice, but not in the whole axon terminal population. Interestingly, mGluR1 and mGluR5 were significantly augmented in total spinal cord tissue already at 60 days. Thus, function and expression of group I mGluRs are enhanced in the early-symptomatic SOD1G93A mouse spinal cord, possibly participating in excessive Glu transmission and supporting their implication in ALS. Please define all abbreviations the first time they appear in the abstract, the main text, and the first figure or table caption.

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