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Ionotropic glutamate receptors interactions

Computational Studies of Ligand-Receptor Interactions in Ionotropic Glutamate Receptors... [Pg.3]

Cover Illustration Figures 2 and 10 from Chapter 1, Computational Studies of Ligand-Receptor Interactions in Ionotropic Glutamate Receptors by Jeremy R. Greenwood and Tommy Liljefors. [Pg.277]

There are three types of ionotropic glutamate receptors NMDA, a-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA), and kainate receptors (Fig. 1). Each is principally activated by the agonist bearing its name and is permeable to cationic flux hence, their activation results in membrane depolarization. Ionotropic glutamate receptors were originally classified based on three selective, synthetic agonists quisqualate, kainate and NMDA. After the discovery of metabotropic receptors, it became clear that quisqualate also interacts with them. Since that time, quisqualate-sensitive ionotropic receptors have been classified by the more selective agonist AMPA. [Pg.253]

Interaction between metabotropic and ionotropic glutamate receptors regulates neuronal network activity. J Neurosci 20 5382-5391. [Pg.483]

Molecular Neuropharmacology Strategies and Methods is intended to bridge the gap between molecular biology and advanced chemistry. In addition, it attempts to include information about x-ray crystallographic analyses whenever available. This book discusses interdisciplinary interactions for monoamine transporters, amino acid transporters, ionotropic receptors, metabotropic glutamate receptors, GABA receptors, and other G protein-coupled receptors. [Pg.278]

Mao L, Wang JQ. 2002. Interactions between ionotropic and metabotropic glutamate receptors regulate cAMP response element-binding protein phosphorylation in cultured striatal neurons. Neuroscience 115 395-402. [Pg.484]

Unfortunately, the impact of anticonvulsants on NA-induced seizures has not been modeled in this way. Given that many coxmtermeasures have different ligand receptor interactions, such an approach would need to be expanded to the other excitatory and inhibitory neurotransmitters and their respective receptors, which are involved in seizure induction and sustainment. However, validation of such an approach, using components of gross EEG recordings, may not be plausible because of the large number of ionotropic channels represented. An endpoint such as sustained elevated glutamate may be more appropriate. [Pg.1043]


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