GluN2B N-methyl-D-aspartic acid receptor subunit mediates atorvastatin-Induced neuroprotection after focal cerebral ischemia

2014 ◽  
Vol 92 (11) ◽  
pp. 1529-1548 ◽  
Author(s):  
Johanna Andrea Gutierrez-Vargas ◽  
Juan Ignacio Muñoz-Manco ◽  
Luis Miguel Garcia-Segura ◽  
Gloria Patricia Cardona-Gómez
Keyword(s):  
Cerebral Ischemia ◽  
Aspartic Acid ◽  
Focal Cerebral Ischemia ◽  
Receptor Subunit ◽  
Acid Receptor

scholarly journals Effect of Ginkgo Biloba Extract on N-Methyl-D-Aspartic Acid Receptor Subunit 2B Expression in a Salicylate-Induced Ototoxicity Model

2019 ◽  
Vol 12 (2) ◽  
pp. 169-175
Author(s):  
Sang-Yeon Lee ◽  
Sang Yoon Han ◽  
Ye-Ji Shim ◽  
Jae-Joon Han ◽  
DeukTae Cho ◽  
...  
Keyword(s):  
Aspartic Acid ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Receptor Subunit ◽  
Acid Receptor

scholarly journals Dorsal Horn α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptor Trafficking in Inflammatory Pain

2010 ◽  
Vol 112 (5) ◽  
pp. 1259-1265 ◽  
Author(s):  
Yuan-Xiang Tao ◽  
David S. Warner
Keyword(s):  
Dorsal Horn ◽  
Aspartic Acid ◽  
Central Sensitization ◽  
Inflammatory Pain ◽  
Persistent Pain ◽  
Receptor Trafficking ◽  
Current Evidence ◽  
Receptor Subunit ◽  
Acid Receptor ◽  
Dorsal Horn Neurons

Activation of synaptic N-methyl-D-aspartic acid receptor and its intracellular downstream signals in dorsal horn neurons of spinal cord contribute to central sensitization, a mechanism that underlies the development and maintenance of pain hypersensitivity in persistent pain. However, the molecular process of this event is not understood completely. Recently, new studies suggest that peripheral inflammatory insults drive changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit trafficking via N-methyl-D-aspartic acid receptor-triggered activation of protein kinases in dorsal horn and raise the possibility that such changes might contribute to central sensitization in persistent pain. This review presents current evidence regarding the changes that occur in the trafficking of dorsal horn alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunits GluR1 and GluR2 under persistent inflammatory pain conditions and discusses the potential mechanisms by which such changes participate in the development and maintenance of inflammatory pain.

Effect of Xingnaojing injection on hippocampal N-methyl-D-aspartic acid receptors of focal cerebral ischemia in rats

2003 ◽  
Vol 9 (1) ◽  
pp. 49-52 ◽  
Author(s):  
Shen Si-yu ◽  
Cai Ding-fang ◽  
Chen Wei-hua ◽  
Liu Jing ◽  
Chen Hu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Aspartic Acid ◽  
Focal Cerebral Ischemia ◽  
Xingnaojing Injection

scholarly journals Maternal Hypothyroxinemia Impairs Spatial Learning and Synaptic Nature and Function in the Offspring

Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 5097-5106 ◽  
Author(s):  
M. C. Opazo ◽  
A. Gianini ◽  
F. Pancetti ◽  
G. Azkcona ◽  
L. Alarcón ◽  
...  
Keyword(s):  
Aspartic Acid ◽  
Spatial Learning ◽  
Water Maze ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Neurological Deficits ◽  
Stratum Radiatum ◽  
Receptor Subunit ◽  
Acid Receptor ◽  
Maze Test

Neurological deficits in the offspring caused by human maternal hypothyroxinemia are thought to be irreversible. To understand the mechanism responsible for these neurological alterations, we induced maternal hypothyroxinemia in pregnant rats. Behavior and synapse function were evaluated in the offspring of thyroid hormone-deficient rats. Our data indicate that, when compared with controls, hypothyroxinemic mothers bear litters that, in adulthood, show prolonged latencies during the learning process in the water maze test. Impaired learning capacity caused by hypothyroxinemia was consistent with cellular and molecular alterations, including: 1) lack of increase of phosphorylated c-fos on the second day of the water maze test; 2) impaired induction of long-term potentiation in response to theta-burst stimulation to the Schaffer collateral pathway in the area 1 of the hippocampus Ammon’s horn stratum radiatum, despite normal responses for input/output experiments; 3) increase of postsynaptic density protein 95 (PSD-95), n-methyl-d-aspartic acid receptor subunit 1, and tyrosine receptor kinase B levels in brain extracts; and 4) significant increase of PSD-95 at the PSDs and failure of this molecule to colocalize with n-methyl-d-aspartic acid receptor subunit 1, as it was shown by control rats. Our findings suggest that maternal hypothyroxinemia is a harmful condition for the offspring that can affect key molecular components for synaptic function and spatial learning.

PPAR-γ agonist rosiglitazone decreases focal cerebral ischemia-induced inflammation and brain damage in adult mice

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S94-S94
Author(s):  
Kudret Tureyen ◽  
Ramya Sundaresan ◽  
Kellie Bowen ◽  
Raghu Vemuganti
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Adult Mice ◽  
Ppar Γ
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