Fetal nerve cell degeneration produced by thalidomide in rabbits

Teratology ◽  
1974 ◽  
Vol 10 (3) ◽  
pp. 283-291 ◽  
Author(s):  
William C. McBride
Keyword(s):  
Nerve Cell ◽  
Cell Degeneration ◽  
Nerve Cell Degeneration

On the role of P2X7 receptors in dopamine nerve cell degeneration in a rat model of Parkinson’s disease: studies with the P2X7 receptor antagonist A-438079

2010 ◽  
Vol 117 (6) ◽  
pp. 681-687 ◽  
Author(s):  
Daniel Marcellino ◽  
Diana Suárez-Boomgaard ◽  
María Dolores Sánchez-Reina ◽  
José A. Aguirre ◽  
Takashi Yoshitake ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Receptor Antagonist ◽  
Nerve Cell ◽  
Rat Model ◽  
P2x7 Receptor ◽  
Cell Degeneration ◽  
P2x7 Receptors ◽  
Nerve Cell Degeneration

Neurotoxin induced nerve cell degeneration: Possible involvement of calcium

1984 ◽  
Vol 295 (2) ◽  
pp. 211-216 ◽  
Author(s):  
Gábor Jancsó ◽  
Sarolta Karcsú ◽  
Elizabeth Király ◽  
Attila Szebeni ◽  
Lajos Tóth ◽  
...  
Keyword(s):  
Nerve Cell ◽  
Cell Degeneration ◽  
Nerve Cell Degeneration

Evidence of active nerve cell degeneration in the substantia nigra of humans years after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine exposure

1999 ◽  
Vol 46 (4) ◽  
pp. 598-605 ◽  
Author(s):  
J. W. Langston ◽  
L. S. Forno ◽  
J. Tetrud ◽  
A. G. Reeves ◽  
J. A. Kaplan ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Nerve Cell ◽  
Cell Degeneration ◽  
Nerve Cell Degeneration

Akabane Disease in Cattle: Congenital Abnormalities caused by Viral Infection. Experimental Disease

1982 ◽  
Vol 19 (3) ◽  
pp. 267-279 ◽  
Author(s):  
S. Konno ◽  
M. Nakagawa
Keyword(s):  
Endothelial Cells ◽  
Congenital Abnormalities ◽  
Akabane Virus ◽  
Cell Degeneration ◽  
Bovine Fetuses ◽  
Reactive Proliferation ◽  
One Year ◽  
Akabane Disease ◽  
Nerve Cell Degeneration ◽  
Experimental Disease

Nonpurulent encephalomyelitis and polymyositis were primary lesions of cattle and goats experimentally infected with Akabane virus. Two caprine fetuses, two months old, were infected placentally and examined 11 days after inoculation; twin caprine fetuses, three months old, were inoculated intramuscularly through the dam's uterus and examined nine days after inoculation. Both lesions were seen in each fetus. Reactive proliferation of immature endothelial cells was a significant encephalitic change. Myositic changes included parenchymal degeneration and cell infiltration in fetuses in the myotubule phase and at the beginning of the myofiber phase. Only nonpurulent encephalomyelitis was seen in six calves 14 days to one year old, inoculated intracerebrally and examined six to 47 days after inoculation. Nerve-cell degeneration, neuroglial mobilization, and perivascular cuffs were typical encephalitic changes in the calves. Five fetuses were infected transplacentally and had polymyositis alone. The four bovine fetuses, two to six months old, were examined nine to 18 days after inoculation, and one caprine fetus, one month old, was examined 11 days after inoculation. Neither encephalomyelitis nor polymyositis was seen in four calves under one year old that were inoculated intravenously.

scholarly journals STUDIES ON PSEUDORABIES (INFECTIOUS BULBAR PARALYSIS, MAD ITCH)

1933 ◽  
Vol 58 (4) ◽  
pp. 415-433 ◽  
Author(s):  
E. Weston Hurst
Keyword(s):  
Nerve Cell ◽  
Glial Cells ◽  
Nerve Cells ◽  
Spinal Ganglia ◽  
Cell Degeneration ◽  
Intracerebral Inoculation ◽  
Bulbar Paralysis ◽  
Nuclear Alterations ◽  
Cardinal Symptom ◽  
In Cells

The histology of pseudorabies differs materially in various animal species. In the rabbit, subcutaneous, intradermal or intramuscular inoculation leads to local inflammation and necrosis. The infection ascends the peripheral nerve (possibly both interstitially and by the axis-cylinders) to the corresponding spinal ganglia and segments of the spinal cord, where primary degeneration of nerve and glial cells takes place. The nerve cell changes are probably responsible for the cardinal symptom of the disease, itching. Death ensues soon after virus reaches the medulla, before visible changes have been produced here. Intracerebral inoculation is followed by characteristic lesions in the meninges, in subpial glial cells and in superficially placed nerve cells. Morbid changes in the lungs are not necessarily related to the presence of virus, but specific lesions may be present. Intranuclear inclusions bearing some resemblance to those in herpetic encephalitis, yellow fever, etc., occur in cells derived from all embryonic layers. The disease in the guinea pig resembles closely that in the rabbit and is modified only by the slightly greater resistance of the animal. In the monkey after intracerebral inoculation, widespread degeneration and necrosis of cortical nerve cells are accompanied by the appearance of specific nuclear alterations in nerve and glial cells, but not in cells of mesodermal origin. No lesions are found in other viscera. In the spontaneous disease in the cow lesions approximate more closely to those in the monkey than to those in the rabbit. In the pig vascular and interstitial lesions predominate, nerve cell degeneration is relatively slight and typical inclusions are not observed. These differences probably explain the benign course of the malady following subcutaneous inoculation in this animal. The lymphatic system, too, participates in the reaction to the virus.

Sign in / Sign up

Export Citation Format

Share Document