(+)-MK 801 maleate
Molecular Weight(MW): 337.37
(+)-MK-801 is a potent, selective and non-competitive NMDA receptor antagonist with Kd of 37.2 nM in rat brain membranes.
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|Description||(+)-MK-801 is a potent, selective and non-competitive NMDA receptor antagonist with Kd of 37.2 nM in rat brain membranes.|
[3H]MK-801 labels high-affinity binding sites in rat cerebral cortical membranes in a saturable manner. MK-801 produces a potent blockade of depolarizing responses to NMDA in rat cerebral cortical slices. The only compounds that are able to compete for [3H]MK-801 binding sites are substances known to block the responses of excitatory amino acids mediated by the NMDA receptor subtype.  MK-801 inhibits N-methyl-D-aspartate-induced [3H]norepinephrine (NE) release and [3H]TCP binding in the hippocampus with IC50 of 20 nM and 9 nM, respectively.  MK-801 causes a progressive, long-lasting blockade of current induced by NMDA. Mg2+ (10 mM) prevents MK-801 from blocking the N-Me-D-Asp-induced current, even when MK-801 is applied for a long time in the presence of NMDA. MK-801 is also effective at blocking NMDA-activated single-channel activity in outside-out patches.  MK-801 (< 500 μM) prevents LPS-induced activation of microglia in a concentration-dependent manner with increased Cox-2 protein expression in BV-2 cells. MK-801 (< 500 μM) reduces microglial TNF-α output with EC50 of 400 μM in BV-2 cells. 
|In vivo||Treatment of mice with MK-801 (1 mg/kg) before each METH injection reduced the extent of DA depletion by 55% in striatal of mice. MK-801 (1 mg/kg) attenuates the effects of METH on microglial activation in striatal of mice.  MK-801 (0.05 mg/kg or 0.2 mg/kg, i.p.) in rats just prior to reactivation of the cocaine-associated memory in the CPP context attenuates subsequent cocaine-primed reinstatement, while no disruption occurres in rats that do not receive reactivation in the CPP context. MK-801 (0.2 mg/kg, i.p.) prior to two reactivation sessions in the home cage does not suppress subsequent cocaine-primed reinstatement. |
-  Wong EH, et al. Proc Natl Acad Sci U S A, 1986, 83(18), 7104-7108.
-  Snell LD, et al. Eur J Pharmacol, 1988, 145(2), 223-226.
-  Huettner JE, et al. Proc Natl Acad Sci U S A, 1988, 85(4), 1307-1311.
|In vitro||DMSO||68 mg/mL (201.55 mM)|
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