dizocilpine-maleate and 3-(2-carboxypiperazine-4-yl)propyl-1-phosphate

dizocilpine-maleate has been researched along with 3-(2-carboxypiperazine-4-yl)propyl-1-phosphate* in 3 studies

Other Studies

3 other study(ies) available for dizocilpine-maleate and 3-(2-carboxypiperazine-4-yl)propyl-1-phosphate

ArticleYear
Low resting potential and postnatal upregulation of NMDA receptors may cause Cajal-Retzius cell death.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999, Mar-01, Volume: 19, Issue:5

    Using in situ patch-clamp techniques in rat telencephalic slices, we have followed resting potential (RP) properties and the functional expression of NMDA receptors in neocortical Cajal-Retzius (CR) cells from embryonic day 18 to postnatal day 13, the time around which these cells normally disappear. We find that throughout their lives CR cells have a relatively depolarized RP (approximately -50 mV), which can be made more hyperpolarized (approximately -70 mV) by stimulation of the Na/K pump with intracellular ATP. The NMDA receptors of CR cells are subjected to intense postnatal upregulation, but their similar properties (EC50, Hill number, sensitivity to antagonists, conductance, and kinetics) throughout development suggest that their subunit composition remains relatively homogeneous. The low RP of CR cells is within a range that allows for the relief of NMDA channels from Mg2+ blockade. Our findings are consistent with the hypothesis that CR cells may degenerate and die subsequent to uncontrolled overload of intracellular Ca2+ via NMDA receptor activation by ambient glutamate. In support of this hypothesis we have obtained evidence showing the protection of CR cells via in vivo blockade of NMDA receptors with dizocilpine.

    Topics: 2-Amino-5-phosphonovalerate; Action Potentials; Adenosine Triphosphate; Aging; Animals; Cell Death; Cerebral Cortex; Dizocilpine Maleate; Embryo, Mammalian; Excitatory Amino Acid Antagonists; Immunohistochemistry; In Vitro Techniques; Meglumine; Membrane Potentials; N-Methylaspartate; Neurons; Neuroprotective Agents; Patch-Clamp Techniques; Piperazines; Rats; Rats, Inbred F344; Receptors, N-Methyl-D-Aspartate; Tetrodotoxin; Up-Regulation

1999
MK-801 blocks monoamine transporters expressed in HEK cells.
    FEBS letters, 1998, Feb-27, Volume: 423, Issue:3

    (+)-MK-801 is known to be a specific non-competitive antagonist of N-methyl-D-aspartate (NMDA) receptors. However, besides having an anticonvulsant effect, this compound possesses a central sympathomimetic effect and an anxiolytic-like action, raising the possibility that (+)-MK-801 might affect monoamine uptake systems. To elucidate this possibility, we investigated the effects of (+)-MK-801 on monoamine transporters expressed in HEK cells. (+)-MK-801 significantly inhibited the uptake of all three monoamine transporters in a dose-dependent manner and the inhibitions were competitive with respect to monoamines. The Ki values of (+)-MK-801 on the norepinephrine, dopamine and serotonin transporters were 3.2 microM, 40 microM and 43 microM, respectively. In addition, (-)-MK-801, a less potent antagonist of NMDA receptors, also inhibited monoamine transporters with a similar potency as that of (+)-MK-801. These results clearly indicate that MK-801, a non-competitive antagonist of NMDA receptors, competitively inhibits monoamine transporters without stereoselectivity.

    Topics: Amino Acid Transport System X-AG; ATP-Binding Cassette Transporters; Binding, Competitive; Biogenic Monoamines; Biological Transport; Carrier Proteins; Cell Line; Dizocilpine Maleate; Dopamine; Dopamine Antagonists; Excitatory Amino Acid Antagonists; Humans; Kidney; Kinetics; Norepinephrine; Piperazines; Receptors, N-Methyl-D-Aspartate; Serotonin; Serotonin Antagonists; Stereoisomerism

1998
The competitive NMDA antagonist CPP blocks MK-801-elicited popping behavior in mice.
    Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 1996, Volume: 15, Issue:4

    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.

    Topics: Animals; Behavior, Animal; Dizocilpine Maleate; Dose-Response Relationship, Drug; Male; Mice; Mice, Inbred Strains; Piperazines; Receptors, N-Methyl-D-Aspartate

1996