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A Neurochemical Approach to Elucidate Metabotropic vs. Ionotropic Glutamate Receptor Activities in Rat Hippocampal Slices
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Darryle D. Schoepp, Manisha A. Desai
Additional studies with NMDA-induced 3H-NE release have aided in the characterization of other modulatory sites on the NMDA receptor complex. For instance, it has been shown that NMDA-induced 3H-NE release in hippocampal slices is inhibited in the presence of physiological concentrations of Mg2+.50–52 Furthermore, various competitive antagonists, including 2-amino-5-phosphonopentanoic acid (AP5), have been shown to induce a parallel shift in the NMDA concentration-response curve.50 It has also been shown that NMDA-induced 3H-NE release is potentiated in the presence of glycine, and that this potentiation of 3H-NE release is inhibited by 7-chlorokynurenic acid, a noncompetitive antagonist that acts at the glycine modulatory site.53 Finally, 3H-NE release has been used as a functional assay to characterize putative competitive antagonists of the polyamine site on the NMDA receptor complex.54,55
Overview of Neurotransmission: Relationship to the Action of Antiepileptic Drugs
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Glycine also has an action at a strychnine-insensitive receptor that has been linked to the NMDA excitatory amino acid receptor.75 This is a high affinity site (Kd for 3H-glycine of 100 to 200 nM) that appears to increase the action of glutamate at its NMDA receptor.123 This strychnine-insensitive glycine binding site has a widespread distribution in brain and seems to be similar to that of the NMDA receptors. Thus, glycine in submicromolar concentrations appears to enhance the action of excitant amino acid neurotransmitters and may even be necessary.123 It appears to enhance excitant amino acid action by binding to a site within the channel and producing an allosteric modification. In this regard it appears to be analogous to the interaction between the GABA receptor and the benzodiazepine binding site. The strychnine-insensitive glycine binding site also appears to have an endogenous antagonist. The tryptophan metabolite, kynurenic acid is an antagonist of the glycine binding site on the NMDA receptor. However, 7-chlorokynurenic acid is a more selective and more potent antagonist and is now being widely used to study this glycine receptor.123
Neurotransmitters and pharmacology
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Ronald A. Browning, Richard W. Clough
As indicated previously, there are no drugs currently available that modulate glycine neurotransmission. The antagonist at the strychnine-insensitive glycine receptor (7-chlorokynurenic acid) may prove to be useful in the future. At present, there is no information on whether or not glycinergic drugs would be useful in the TBI patient.
Molecular mechanisms that change synapse number
Published in Journal of Neurogenetics, 2018
Alicia Mansilla, Sheila Jordán-Álvarez, Elena Santana, Patricia Jarabo, Sergio Casas-Tintó, Alberto Ferrús
It is well established that activity-induced shrinkage and retraction of dendritic spines depend on activation of the NMDA-type glutamate receptor (NMDAR), which leads to influx of extracellular Ca2+ ions and activation of Ca2+-dependent phosphatases that modify the spine cytoskeleton, suggesting that influx of extracellular Ca2+ drives spine shrinkage. However, non-ionotropic function of the NMDAR also regulates synaptic strength (Nabavi et al., 2013). Additional support to this phenomenon has been obtained by two-photon glutamate uncaging and time-lapse imaging of rat hippocampal CA1 neurons, in the presence of the NMDAR d-serine/glycine binding site antagonist 7-chlorokynurenic acid (7CK), which blocks the Ca2+ influx (Stein, Gray, & Zito, 2015).