NDLI: Effects of β-Amyloid-(25-35) Peptides on Radioligand Binding to Excitatory Amino Acid Receptors and Voltage-Dependent Calcium Channels: Evidence for a Selective Affinity for the Glutamate and Glycine Recognition Sites of the NMDA Receptor

Content Provider	Springer Nature Link
Author	Cowburn, Richard F. Wiehager, Birgitta Trief, Ewa Li Li, Mo Sundström, Erik
Copyright Year	1997
Abstract	The neurotoxic fragment corresponding to residues 25-35 of the β-amyloid (Aβ) peptide [Aβ-(25-35)] has been shown to exert effects on (+)-[$^{3}$H]5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine maleate ([$^{3}$H]MK-801) binding to the cation channel of the N-methyl-D-aspartate (NMDA) receptor. In the present study, we investigated whether the amidated and carboxylic acid C-terminated forms of Aβ-(25-35) [Aβ-(25-35-NH$_{2}$) and Aβ-(25-35-COOH), respectively] exert effects on other excitatory amino acid receptor and cation channel types in rat cortical membranes. Both Aβ-(25-35-NH$_{2}$) and Aβ-(25-35-COOH) gave statistically significant dose-dependent inhibitions of [$^{3}$H]glutamate and [$^{3}$H]glycine binding to the agonist recognition sites of the NMDA receptor. Ten μM Aβ-(25-35-NH$_{2}$) and Aβ-(25-35-COOH) gave 25% and 20% inhibitions of [$^{3}$H]glutamate binding and 75% and 70% inhibitions of [$^{3}$H]glycine binding, respectively. Aβ-(25-35-NH$_{2}$), but not Aβ-(25-35-COOH), gave a small (ca. 17% at 10 μM) statistically significant increase of [$^{3}$H]amino-3-hydroxy-5-methylisoxazole-4-propionate ([$^{3}$H]AMPA) binding. [$^{3}$H]kainate binding was not significantly affected by either peptide. Similarly, neither peptide affected either the maximal level or EC$_{50}$ value for calcium stimulation of [$^{3}$H]nitrendipine binding. It is concluded that Aβ-(25-35) shows slight affinity for the agonist recognition sites of the NMDA receptor, but not for other excitatory amino acid receptor types or for L-type voltage-dependent calcium channels.
Starting Page	1437
Ending Page	1442
Page Count	6
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	22
Issue Number	12
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	1997-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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Involvement of NMDA Receptor in the Modulation of Excitatory and Inhibitory Amino Acid Neurotransmitters Release in Cortical Neurons

Glutamate receptors function as scaffolds for the regulation of β-amyloid and cellular prion protein signaling complexes

β-Amyloid 25-35 Peptide Reduces the Expression of Glutamine Transporter SAT1 in Cultured Cortical Neurons

Genistein alleviates the mitochondria-targeted DNA damage induced by β-amyloid peptides 25–35 in C6 glioma cells

Downregulation of calcium-dependent NMDA receptor desensitization by sodium-calcium exchangers: a role of membrane cholesterol

Ca2+/Calmodulin-dependent protein Kinase II interacts with group I Metabotropic Glutamate and facilitates Receptor Endocytosis and ERK1/2 signaling: role of β-Amyloid

Cl-/Ca2+-dependent L-glutamate binding sites do not correspond to 2-amino-4-phosphonobutanoate-sensitive excitatory amino acid receptors.

Selective mGluR5 antagonists MPEP and SIB-1893 decrease NMDA or glutamate-mediated neuronal toxicity through actions that reflect NMDA receptor antagonism.

Extracellular Calcium Modulates Actions of Orthosteric and Allosteric Ligands on Metabotropic Glutamate Receptor 1α

Effects of β-Amyloid-(25-35) Peptides on Radioligand Binding to Excitatory Amino Acid Receptors and Voltage-Dependent Calcium Channels: Evidence for a Selective Affinity for the Glutamate and Glycine Recognition Sites of the NMDA Receptor

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