Disclosure by triton X-100 of NMDA-sensitive [3H] glutamate binding sites in brain synaptic membranes.
Pretreatment of brain synaptic membrane homogenates with Triton X-100 resulted in a drastic disclosure of [3H] glutamate (Glu) binding activity which was sensitive to one of the central Glu receptor agonists, N-methyl-D-aspartic acid (NMDA). The NMDA-sensitive binding was inversely dependent on the incubation temperature, and was a reversible and saturable process. Scatchard analysis revealed that Triton X-100 treatment yielded in a significant enhancement of the affinity with a concomitant increment of the density of binding sites. Electrophysiologically identified agonists and antagonists for the NMDA receptors all significantly inhibited the binding to Triton-treated membranes. These results suggest that Triton-treatment may disclose NMDA-sensitive [3H] Glu binding sites in brain synaptic membranes.
Ogita
K
K
Department of Pharmacology, Setsunan University, Osaka, Japan.
Yoneda
Y
Y
D000596:Amino Acids / Q000378:metabolism; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D001667:Binding, Competitive; D001921:Brain / Q000378:metabolism*; D005971:Glutamates / Q000502:physiology*; D066298:In Vitro Techniques; D007700:Kinetics; D008722:Methods; D016202:N-Methylaspartate; D017830:Octoxynol; D011092:Polyethylene Glycols / Q000494:pharmacology*; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism*; D013570:Synaptic Membranes / Q000378:metabolism; D013696:Temperature
D000596:Amino Acids; D005971:Glutamates; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter; D001224:Aspartic Acid; D011092:Polyethylene Glycols; D016202:N-Methylaspartate; D017830:Octoxynol