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Characterization of spermidine-dependent [3H](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) binding in brain synaptic membranes treated with Triton X-100.

Addition of spermidine (SPD) at concentrations above 10 microM markedly potentiated the binding of a radiolabeled noncompetitive antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) for an N-methyl-D-aspartate (NMDA)-sensitive subclass of central excitatory amino acid neurotransmitter receptors in the presence of 10 microM glutamic acid (Glu) in brain synaptic membranes treated with 0.08% Triton X-100. Both spermine and bis-(3-aminopropyl)amine also potentiated the binding at a concentration over 10 microM, with the other polyamines examined being ineffective at similar concentrations. Glycine (Gly) at 10 microM additionally potentiated the binding through accelerating the initial association rate without affecting the binding at equilibrium in the presence of Glu alone, whereas SPD at 1 mM increased both the association rate and steady-state level found in the presence of Glu alone. This potentiation by SPD in the presence of Glu was not only prevented by competitive NMDA antagonists, but also antagonized by antagonists highly selective for strychnine-insensitive binding sites of Gly. Further addition of Gly reversed the inhibition by Gly antagonists without affecting that by NMDA antagonists. The SPD-dependent binding was significantly inhibited by various proteases and phospholipases, but not by glycosidases at the concentrations used. All brain regions examined had similar affinities for [3H]MK-801 with different densities of [3H]MK-801 binding sites when determined in the presence of both Glu and Gly. Further addition of SPD failed to affect either the affinity or density in the cerebellum, with the affinity being increased in the rest parts of rat brain. These results suggest that SPD may elicit a stimulatory action on the binding of [3H]MK-801 to open NMDA channels in a manner dependent on the NMDA recognition sites that absolutely require Gly for activation in the brain. The present findings are also suggestive of heterogeneity of the NMDA receptor complex in terms of the differential sensitivity to potentiation by SPD.