The competitive NMDA antagonist CPP blocks MK-801-elicited popping behavior in mice.
In the current investigation, the ability of CPP (3-(2-carboxypiperazine-4-yl) propyl-1-phosphate) to elicit mouse popping behavior in a manner similar to that of MK-801 was studied. Unlike MK-801, CPP (3.2-32 mg/kg) did not elicit any popping. The data show that a reduction in NMDA-mediated neural transmission alone is not sufficient to elicit popping behavior in mice. Moreover, pretreatment of mice with CPP attenuated MK-801's ability to elicit popping. These results suggest that popping requires the channel to be in the "active", or open, configuration and that it depends on MK-801's access and binding to its unique site in the hydrophobic channel domain.
Department of Veterans Affairs Medical Center, Washington, DC 20422, USA.
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Deutsch
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Rosse
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Riggs
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Koetzner
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Mastropaolo
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D016291:Dizocilpine Maleate / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010879:Piperazines / Q000494:pharmacology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*
D010879:Piperazines; D016194:Receptors, N-Methyl-D-Aspartate; C104291:3-(2-carboxypiperazine-4-yl)propyl-1-phosphate; D016291:Dizocilpine Maleate