AMINO ACID ANTAGONISTS

2010 ◽  
pp. 59-64
Keyword(s):  
Amino Acid ◽  
Amino Acid Antagonists

Amino Acid Antagonists

2018 ◽  
pp. 191-194
Keyword(s):  
Amino Acid ◽  
Amino Acid Antagonists

Effects ofin situadministration of excitatory amino acid antagonists on rapid microglial and astroglial reactions in rat hippocampus following traumatic brain injury

2008 ◽  
Vol 30 (4) ◽  
pp. 420-429 ◽  
Author(s):  
Takeshi Suma ◽  
Morimichi Koshinaga ◽  
Masamichi Fukushima ◽  
Tsuneo Kano ◽  
Yoichi Katayama
Keyword(s):  
Traumatic Brain Injury ◽  
Amino Acid ◽  
Brain Injury ◽  
Excitatory Amino Acid ◽  
Rat Hippocampus ◽  
Amino Acid Antagonists ◽  
Excitatory Amino Acid Antagonists

Stereochemistry and Tautomerism of Amino Acid Antagonists: α,γ-Diketo Acids and Esters and their Cyclisation Products

1983 ◽  
Vol 38 (2) ◽  
pp. 220-225 ◽  
Author(s):  
W. S. Sheldrick ◽  
W. Trowitzsch
Keyword(s):  
Amino Acid ◽  
Methyl Ester ◽  
Glyoxylic Acid ◽  
Acid Methyl Ester ◽  
Acid Ethyl Ester ◽  
Enolic Form ◽  
X Ray ◽  
Acid Methyl ◽  
Acid Proton ◽  
Amino Acid Antagonists

Abstract X-ray structural analyses of two α,γ-diketo esters and one α,γ-diketo acid, which are amino acid antagonists, have shown them all to be present in the solid state in the α,β-unsaturated γ-keto enolic form. The structures of the esters β-acetyl-pyruvic acid methyl ester (1) and 2-oxo-cyclopentyl-glyoxylic acid ethyl ester (3) are stabilized by intra-molecular O···H(-O) hydrogen bonds involving the enol proton. In the case of camphor oxalic acid (4) an intramolecular O···H-O hydrogen bond between the γ-keto oxygen and the acid proton is observed. The bond lengths and angles in 1 indicate a significant contribution from the mesomeric β,γ-unsaturated enol form. For comparison purposes the structure of the γ-enol methyl ether of 1, (4-methoxy-2-oxo-pentene)carboxylic acid methyl ester (2) has also been determined. The X-ray structures of the cyclization products of respectively an α,γ-diketo acid and an α,γ-diketo ester are reported.

STRUCTURE AND CONFORMATION OF AMINO-ACID ANTAGONISTS

1981 ◽  
pp. 621-631
Author(s):  
K.K. CHACKO ◽  
S. SWAMINATHAN ◽  
S.K. BHATTACHARJEE
Keyword(s):  
Amino Acid ◽  
Amino Acid Antagonists

Behavioural and eeg effects of some excitatory amino acid antagonists

1988 ◽  
Vol 20 (5) ◽  
pp. 409-410 ◽  
Author(s):  
M. Benedetti ◽  
S. Sagratella ◽  
A. Scotti de Carolis
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Amino Acid Antagonists ◽  
Excitatory Amino Acid Antagonists

scholarly journals Administration of Excitatory Amino Acid Antagonists via Microdialysis Attenuates the Increase in Glucose Utilization Seen following Concussive Brain Injury

1992 ◽  
Vol 12 (1) ◽  
pp. 12-24 ◽  
Author(s):  
Tatsuro Kawamata ◽  
Yoichi Katayama ◽  
David A. Hovda ◽  
Atsuo Yoshino ◽  
Donald P. Becker
Keyword(s):  
Amino Acid ◽  
Brain Injury ◽  
Ion Channels ◽  
Energy Demand ◽  
Glucose Utilization ◽  
Excitatory Amino Acid ◽  
Ionic Balance ◽  
Ionic Fluxes ◽  
Amino Acid Antagonists ◽  
Concussive Injury

Immediately following concussive brain injury, cells exhibit an increase of energy demand represented by the activation of glucose utilization. We have proposed that this trauma-induced hypermetabolism reflects the effort of cells to restore normal ionic balance disrupted by massive ionic fluxes through transmitter-gated ion channels. In the present study, changes in local CMRglc following fluid-percussion concussive injury were determined using [14C]2-deoxy-d-glucose autoradiography, and the effects of in situ administration (via microdialysis) of excitatory amino acid (EAA) antagonists [kynurenic acid (KYN), 2-amino-5-phosphonovaleric acid (APV; 100 μ M, 1 m M, and 10 m M), and 6-cyano-7-nitroquinoxaline-2,3-dine (CNQX; 300 μ M, 1 m M, and 10 m M] on glucose utilization were investigated. Animals that did not receive dialysis showed a remarkable increase (up to 181% of normal control) in cortical glucose utilization following injury. In contrast, this high demand for glucose was reduced in areas infiltrated with KYN, APV, and CNQX. These results indicate that EAA-activated ion channels are involved in the posttraumatic increase in glucose utilization, reflecting the energy demand of cells required to drive pumping mechanisms against an ionic perturbation seen immediately following the concussive injury. The effects of KYN, APV, and CNQX suggest that although all subtypes of the glutamate receptor appear to be involved in this phenomenon, N-methyl-d-aspartate-activated channels may play a major role.

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