Abstract
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.
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Deutsch, S., Rosse, R., Riggs, R. et al. The Competitive NMDA Antagonist CPP Blocks MK-801-Elicited Popping Behavior in Mice. Neuropsychopharmacol 15, 329–331 (1996). https://doi.org/10.1016/0893-133X(95)00236-7
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DOI: https://doi.org/10.1016/0893-133X(95)00236-7
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