Neurotrophin Expression in Nerve Agent VX-Exposed Rat Brain

2007 ◽  
Author(s):  
Santresda M. Johnson ◽  
Chris L. Robison ◽  
Tsung-Ming A. Shih ◽  
Lawrence Tong ◽  
Sarah Parylak ◽  
...  
Keyword(s):  
Rat Brain ◽  
Nerve Agent

Regional alterations of JNK3 and CaMKIIα subunit expression in the rat brain after soman poisoning

2010 ◽  
Vol 30 (6) ◽  
pp. 448-459 ◽  
Author(s):  
G. RamaRao ◽  
CK Waghmare ◽  
Nalini Srivastava ◽  
BK Bhattacharya
Keyword(s):  
Cerebral Cortex ◽  
Protein Kinase ◽  
Rat Brain ◽  
Protein Kinases ◽  
Nerve Agent ◽  
Dependent Protein Kinase ◽  
Altered Expression ◽  
Calcium Calmodulin Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein

Calcium/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinases (JNKs) exert numerous and diverse functions in the brain. However, their role in nerve agent poisoning is poorly understood. In the present study, rats were exposed to soman (80 µg/kg) subcutaneously to study the changes in the protein levels of calcium/calmodulin-dependent protein kinase II alpha subunit (CaMKIIα) and JNK3 and activities of acetylcholinestarase (AChE) and CaMKII in the rat brain. Western blot analysis revealed that significant changes were found in both the protein kinases expression. Immunoreactivity levels of neural specific JNK3 isoform increased from 2.5 hours to 30 days after soman exposure in cerebral cortex, hippocampus, striatum and thalamus regions and decreased in the case of cerebellum. CaMKIIα expression levels were also increased from 2.5 hours to 30 days after soman exposure in cerebral cortex, hippocampus, thalamus and down regulated in cerebellum. AChE activity remained inhibited in plasma and brain up to 3 days post exposure. CaMKII activity was increased in cerebrum and decreased in cerebellum. Results suggest that altered expression of both the protein kinases play a role in nerve agent-induced long-term neurotoxic effects.

scholarly journals A Comparison of the Potency of the Oxime HLö-7 and Currently Used Oximes (HI-6, Pralidoxime, Obidoxime) to Reactivate Nerve Agent-Inhibited Rat Brain Acetylcholinesterase by in vitro Methods

2005 ◽  
Vol 48 (2) ◽  
pp. 81-86 ◽  
Author(s):  
Kamil Kuča ◽  
Jiří Cabal ◽  
Jiří Kassa ◽  
Daniel Jun ◽  
Martina Hrabinová
Keyword(s):  
Rat Brain ◽  
Nerve Agents ◽  
Nerve Agent ◽  
The Other ◽  
In Vitro Evaluation ◽  
In Vitro Methods ◽  
Hi 6 ◽  
Hlö 7 ◽  
Brain Acetylcholinesterase

1. The efficacy of the oxime HLö-7 and currently used oximes (pralidoxime, obidoxime, HI-6) to reactivate acetylcholinesterase inhibited by various nerve agents (sarin, tabun, cyclosarin, VX) was tested by in vitro methods. 2. Both H oximes (HLö-7, HI-6) were found to be more efficacious reactivators of sarin and VX-inhibited acetylcholinesterase than pralidoxime and obidoxime. On the other hand, their potency to reactivate tabun-inhibited acetylcholinesterase is very low and does not reach the reactivating efficacy of obidoxime. In the case of cyclosarin, the oxime HI-6 was only found to be able to sufficiently reactivate cyclosarin-inhibited acetylcholinesterase in vitro. 3. Thus, the oxime HLö-7 does not seem to be more efficacious reactivator of nerve agent-inhibited acetylcholinesterase than HI-6 according to in vitro evaluation of their reactivation potency and, therefore, it is not more suitable to be introduced for antidotal treatment of nerve agent-exposed people than HI-6.

cDNA cloning and expression of a gamma-aminobutyric acidA receptor epsilon-subunit in rat brain

2000 ◽  
Vol 12 (12) ◽  
pp. 4318-4330 ◽  
Author(s):  
Nathalie Moragues ◽  
Philippe Ciofi ◽  
Pierrette Lafon ◽  
Marie-Francoise Odessa ◽  
Gerard Tramu ◽  
...  
Keyword(s):  
Rat Brain ◽  
Cdna Cloning ◽  
Cloning And Expression ◽  
Epsilon Subunit

Antisense knockdown of the glial glutamate transporter GLT-1 exacerbates hippocampal neuronal damage following traumatic injury to rat brain

2001 ◽  
Vol 13 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Vemuganti L. Raghavendra Rao ◽  
Aclan Dogan ◽  
Kellie K. Bowen ◽  
Kathryn G. Todd ◽  
Robert J. Dempsey
Keyword(s):  
Rat Brain ◽  
Neuronal Damage ◽  
Traumatic Injury ◽  
Glutamate Transporter ◽  
Glial Glutamate Transporter ◽  
Antisense Knockdown

Inhibition of Rat Brain Monoamine Oxidase Activities by Psoralen and Isopsoralen: Implications for the Treatment of Affective Disorders

2001 ◽  
Vol 88 (2) ◽  
pp. 75-80 ◽  
Author(s):  
Ling Dong Kong ◽  
Ren Xiang Tan ◽  
Anthony Yiu Ho Woo ◽  
Christopher Hon Ki Cheng2Note
Keyword(s):  
Monoamine Oxidase ◽  
Rat Brain ◽  
Affective Disorders ◽  
Brain Monoamine
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