Ultrastructural alterations of neuronal cells in a brain stem ganglioglioma

1987 ◽  
Vol 74 (3) ◽  
pp. 307-312 ◽  
Author(s):  
H. Takahashi ◽  
F. Ikuta ◽  
T. Tsuchida ◽  
R. Tanaka
Keyword(s):  
Brain Stem ◽  
Neuronal Cells ◽  
Ultrastructural Alterations

NT-4 protein is localized in neuronal cells in the brain stem as well as the dorsal root ganglion of embryonic and adult rats

2003 ◽  
Vol 86 (3) ◽  
pp. 660-668 ◽  
Author(s):  
Ritsuko Katoh-Semba ◽  
Satoshi Ichisaka ◽  
Yoshio Hata ◽  
Tadaharu Tsumoto ◽  
Kazuyo Eguchi ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Brain Stem ◽  
Dorsal Root ◽  
Neuronal Cells ◽  
Adult Rats ◽  
The Brain

Anaplastic ganglioglioma of the brain stem demonstrating active neurosecretory features of neoplastic neuronal cells

1992 ◽  
Vol 83 (4) ◽  
pp. 365-370 ◽  
Author(s):  
T. Hirose ◽  
S. Kannuki ◽  
K. Nishida ◽  
K. Matsumoto ◽  
T. Sano ◽  
...  
Keyword(s):  
Brain Stem ◽  
Neuronal Cells ◽  
The Brain

Permeability of the microcirculation in area postrema of rat

1988 ◽  
Vol 46 ◽  
pp. 348-349
Author(s):  
Shams M. Ghoneim ◽  
Frank M. Faraci ◽  
Gary L. Baumbach
Keyword(s):  
Brain Stem ◽  
Area Postrema ◽  
Upper Body ◽  
Sprague Dawley ◽  
Sodium Cacodylate ◽  
Acute Hypertension ◽  
Sprague Dawley Rats ◽  
Ultrastructural Characteristics ◽  
The Brain ◽  
Adjacent Brain

The area postrema is a circumventricular organ in the brain stem and is one of the regions in the brain that lacks a fully functional blood-brain barrier. Recently, we found that disruption of the microcirculation during acute hypertension is greater in area postrema than in the adjacent brain stem. In contrast, hyperosmolar disruption of the microcirculation is greater in brain stem. The objective of this study was to compare ultrastructural characteristics of the microcirculation in area postrema and adjacent brain stem.We studied 5 Sprague-Dawley rats. Horseradish peroxidase was injected intravenously and allowed to circulate for 1, 5 or 15 minutes. Following perfusion of the upper body with 2.25% glutaraldehyde in 0.1 M sodium cacodylate, the brain stem was removed, embedded in agar, and chopped into 50-70 μm sections with a TC-Sorvall tissue chopper. Sections of brain stem were incubated for 1 hour in a solution of 3,3' diaminobenzidine tetrahydrochloride (0.05%) in 0.05M Tris buffer with 1% H2O2.

Ultrastructural Alterations in Sinusoidal Endothelial Fenestrae as a Result of Hypoxia

1976 ◽  
Vol 34 ◽  
pp. 168-169
Author(s):  
Waykin Nopanitaya ◽  
Raeford E. Brown ◽  
Joe W. Grisham ◽  
Johnny L. Carson
Keyword(s):  
Endothelial Cells ◽  
Experimental Model ◽  
Hepatic Lobule ◽  
Ultrastructural Alterations ◽  
Large Type ◽  
Sinusoidal Endothelial Fenestrae ◽  
General Size ◽  
Sem Studies

Mammalian endothelial cells lining hepatic sinusoids have been found to be widely fenestrated. Previous SEM studies (1,2) have noted two general size catagories of fenestrations; large fenestrae were distributed randomly while the small type occurred in groups. These investigations also reported that large fenestrae were more numerous and larger in the endothelial cells at the afferent ends of sinusoids or around the portal areas, whereas small fenestrae were more numerous around the centrilobular portion of the hepatic lobule. It has been further suggested that under some physiologic conditions small fenestrae could fuse and subsequently become the large type, but this is, as yet, unproven.We have used a reproducible experimental model of hypoxia to study the ultrastructural alterations in sinusoidal endothelial fenestrations in order to investigate the origin of occurrence of large fenestrae.

Surgical Approaches to the Brain Stem

1993 ◽  
Vol 4 (3) ◽  
pp. 457-468 ◽  
Author(s):  
Dennis Y. Wen ◽  
Roberto C. Heros
Keyword(s):  
Brain Stem ◽  
Surgical Approaches ◽  
The Brain

Cytoprotective Effect of Tocotrienol-Rich Fraction and α-Tocopherol Vitamin E Isoforms Against Glutamate-Induced Cell Death in Neuronal Cells

2014 ◽  
Vol 84 (3-4) ◽  
pp. 0140-0151 ◽  
Author(s):  
Thilaga Rati Selvaraju ◽  
Huzwah Khaza’ai ◽  
Sharmili Vidyadaran ◽  
Mohd Sokhini Abd Mutalib ◽  
Vasudevan Ramachandran ◽  
...  
Keyword(s):  
Vitamin E ◽  
Cell Viability ◽  
Neuronal Cells ◽  
Positive Control ◽  
Post Treatment ◽  
Mitochondrial Activity ◽  
Before And After ◽  
Pre Treatment ◽  
Tocotrienol Rich Fraction ◽  
Major Mediator

Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. We aimed to clarify the potential of the following vitamin E isomers, tocotrienol-rich fraction (TRF) and α-tocopherol (α-TCP), as potent neuroprotective agents against glutamate-induced injury in neuronal SK-N-SH cells. Cells were treated before and after glutamate injury (pre- and post-treatment, respectively) with 100 - 300 ng/ml TRF/α-TCP. Exposure to 120 mM glutamate significantly reduced cell viability to 76 % and 79 % in the pre- and post-treatment studies, respectively; however, pre- and post-treatment with TRF/α-TCP attenuated the cytotoxic effect of glutamate. Compared to the positive control (glutamate-injured cells not treated with TRF/α-TCP), pre-treatment with 100, 200, and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 95.2 %, 95.0 %, and 95.6 %, respectively (p < 0.05).The isomers not only conferred neuroprotection by enhancing mitochondrial activity and depleting free radical production, but also increased cell viability and recovery upon glutamate insult. Our results suggest that vitamin E has potent antioxidant potential for protecting against glutamate injury and recovering glutamate-injured neuronal cells. Our findings also indicate that both TRF and α-TCP could play key roles as anti-apoptotic agents with neuroprotective properties.

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