scholarly journals Central nervous system uptake kinetics of pentylenetetrazol in the developing rat

1991 ◽  
Vol 12 (1) ◽  
pp. 59-71 ◽  
Author(s):  
Lynda J. Haberer ◽  
Gary M. Pollack
1992 ◽  
Vol 70 (11) ◽  
pp. 1515-1518 ◽  
Author(s):  
B. Skrajny ◽  
R. S. Hannah ◽  
S. H. Roth

The central nervous system is one of the primary target organs for hydrogen sulphide (H2S) toxicity; however, there are limited data on the neurotoxic effects of low-dose chronic exposure on the developing nervous system. Levels of serotonin and norepinephrine in the developing rat cerebellum and frontal cortex were determined following chronic exposure to 20 and 75 ppm H2S during perinatal development. Both monoamines were altered in rats exposed to 75 ppm H2S compared with controls; serotonin levels were significantly increased at days 14 and 21 postnatal in both brain regions, and norepinephrine levels were significantly increased at days 7, 14, and 21 postnatal in cerebellum and at day 21 in the frontal cortex. Exposure to 20 ppm H2S significantly increased the levels of serotonin in the frontal cortex at day 21, whereas levels of norepinephrine were significantly reduced in the frontal cortex at days 14 and 21, and at day 14 in the cerebellum.Key words: hydrogen sulphide, monoamines, serotonin, norepinephrine, neurotoxicity.


1988 ◽  
Vol 459 (1) ◽  
pp. 200-203 ◽  
Author(s):  
John W. McDonald ◽  
Faye S. Silverstein ◽  
Michael V. Johnston

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Birte Eikeland

Research in the last few years has indicated that most voltage-gated potassium channel- (VGKC-) complex antibodies without leucine-rich glioma-inactivated protein 1 or contactin-associated protein-like 2 antibody specificity lack pathogenic potential and are not clear markers for autoimmune inflammation. Here we report on a patient with double-negative VGKC who developed severe peripheral nerve hyperexcitability, central nervous system symptoms with agitation and insomnia, dysautonomia, and systemic symptoms with weight loss, itch, and skin lesions. The disease started acutely one month after an episode of enteroviral pericarditis and responded well to immunotherapy. The patient is presumed to have developed a postinfectious immunotherapy-responsive autoimmune disease. In the setting of anti-VGKC positivity, it seems likely that anti-VGKC contributed to the pathogenesis of the patient’s symptoms of nerve hyperexcitability and that the disease was caused by an acquired autoimmune effect on the neuronal kinetics of VGKC. It is still unknown whether or not there are unidentified extracellular molecular targets within the VGKC-complex, i.e., a novel surface antigen and a pathogenic antibody that can cause affected individuals to develop a peripheral nerve hyperexcitability syndrome. This case highlights the fact that less well-characterized autoimmune central and peripheral nervous system syndromes may have infectious triggers.


1962 ◽  
Vol 203 (4) ◽  
pp. 739-747 ◽  
Author(s):  
Charles R. Kleeman ◽  
Hugh Davson ◽  
Emanuel Levin

The kinetics of urea transport in the central nervous system have been studied in rabbits during sustained intravenous and intracisternal infusions of C12 and C14 urea. The steady state content of urea in the water phase of the white matter and cord was approximately equal to its content in plasma water. However, the water of whole brain and gray matter had levels of urea which exceeded those in plasma by 7 and 18%, respectively, whereas the urea in cerebrospinal fluid (CSF) was only 78% of the plasma level. Its rate of penetration into nervous tissue was approximately one-tenth as rapid as into muscle. The intravenous infusion of urea caused a significant decrease in water content of the brain and cord. It was estimated that urea infused into the subarachnoid space penetrated the central nervous system (CNS) tissues at four to five times the rate of transport from blood to CNS tissues. These studies suggest that intravenous infusions of urea lower CSF pressure by decreasing the volume of the brain and cord. The major barrier to urea penetration into nervous tissue is at the capillary level, and not the plasma membrane of the glial or neuronal cells.


2000 ◽  
Vol 120 (1) ◽  
pp. 83-86 ◽  
Author(s):  
P.E Pomata ◽  
A.A Colman-Lerner ◽  
J.L Barañao ◽  
M.L Fiszman

1998 ◽  
Vol 11 (2) ◽  
pp. 133-133 ◽  
Author(s):  
Dong-ping Lu ◽  
Hiroyuki Nakayama ◽  
Junko Shinozuka ◽  
Koji Uetsuka ◽  
Ryuichi Taki ◽  
...  

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