Interaction of the NMDA receptor noncompetitive antagonist MK-801 with model and native membranes

Moring, J.; Niego, L.A.; Ganley, Lisa; Trumbore, Mark W.

doi:10.1016/s0006-3495(94)80724-6

Cited by 15 publications

(14 citation statements)

References 44 publications

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“…Further, these compounds differ in their binding site. While memantine is believed to bind at or near the Mg 2+ binding site (Chen and Lipton 1997; Chen et al 1992), MK-801 binds to the PCP site inside the pore of the receptor (Moring et al 1994; Sakurada et al 1993). Despite differing pharmacological profiles, these two drugs produced the same behavioral effects of blocking consolidation and interfering with the reconsolidation of cocaine-cue memories.…”

Section: Discussionmentioning

confidence: 99%

Common influences of non-competitive NMDA receptor antagonists on the consolidation and reconsolidation of cocaine-cue memory

Alaghband

Marshall

2012

Psychopharmacology

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Rationale Environmental stimuli or contexts previously associated with rewarding drugs contribute importantly to relapse among addicts, and research has focused on neurobiological processes maintaining those memories. Much research shows contributions of cell surface receptors and intracellular signaling pathways in maintaining associations between rewarding drugs (e.g., cocaine) and concurrent cues/contexts; these memories can be degraded at the time of their retrieval through reconsolidation interference. Much less studied is the consolidation of drug-cue memories during their acquisition. Objective The present experiments use the cocaine conditioned place preference (CPP) paradigm in rats to directly compare, in a consistent setting, the effects of N-methyl-D-aspartate (NMDA) glutamate receptor antagonists MK-801 and memantine on the consolidation and reconsolidation of cocaine-cue memories. Methods For the consolidation studies, animals were systemically administered MK-801 or memantine immediately following training sessions. To investigate the effects of these NMDA receptor antagonists on the retention of previously-established cocaine-cue memories, animals were systemically administered MK-801 or memantine immediately after memory retrieval. Results Animals given either NMDA receptor antagonist immediately following training sessions did not establish a preference for the cocaine-paired compartment. Post-retrieval administration of either NMDA receptor antagonist attenuated the animals' preference for the cocaine-paired compartment. Furthermore, animals given NMDA receptor antagonists post-retrieval showed a blunted response to cocaine-primed reinstatement. Conclusions Using two distinct NMDA receptor antagonists in a common setting, these findings demonstrate that NMDA receptor-dependent processes contribute both to the consolidation and reconsolidation of cocaine-cue memories, and they point to the potential utility of treatments that interfere with drug-cue memory reconsolidation.

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Section: Discussionmentioning

confidence: 99%

Common influences of non-competitive NMDA receptor antagonists on the consolidation and reconsolidation of cocaine-cue memory

Alaghband

Marshall

2012

Psychopharmacology

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“…With the exception of Purkinje cell counts in the cerebellum, intermediate effects between the (+)MK-801 and saline-treated mutants were observed when the less effective isomer (-)MK-801 (seven times weaker binding affinity) [Wong et al, 1986;Moring et al, 1994] was used to treat the mutants. Further, administration of ketamine, which has a 300-fold lower binding affinity to the NMDA receptor as compared to MK-801 [Wong et al, 1988], resulted in a reduced, yet intermediate level of neuroprotection in the cerebellum.…”

Section: Discussionmentioning

confidence: 99%

Effect of the Noncompetitive NMDA Antagonists MK-801 and Ketamine on the <i>Spastic</i> Han-Wistar Mutant: A Rat Model of Excitotoxicity

Brunson

Khanna²,

Cromwell³

et al. 2001

Dev Neurosci

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The neuroprotective effects of the NMDA antagonists MK-801 and ketamine were analyzed in a mutant strain of Han-Wistar rats which develop neurodegeneration in the hippocampus and cerebellum. Previous experiments have shown that the progressive neuronal degeneration observed in this mutant may be the result of a dysfunctional glutamatergic system. For MK-801 studies, mutants were injected in a chronic paradigm with (+)MK-801 or its weaker acting isomer (–)MK-801 at a dose of 1 mg/kg. Ketamine studies consisted of both acute (50 mg/kg once) and chronic (10 mg/kg multiple times) injection paradigms. MK-801-treated mutants exhibited longer life spans (8–23%) compared to saline-injected mutants. Ketamine-injected mutants in both paradigms also lived slightly longer (6–9%) than the saline mutants. Motor skill deterioration was monitored in an open-field test, and after 50 days of age the MK-801 and ketamine mutants displayed over 20% greater motor skill activity than the saline mutants. In the cerebellum, mutants treated with ketamine and both forms of MK-801 had 10–20% more Purkinje cells surviving at 55 days than the saline mutants. Further, the density of CA3c pyramidal hippocampal neurons in ketamine and MK-801-treated mutants as compared to saline mutants appeared to be greater upon qualitative analysis. This study shows that these mutants derive some protective effects from the NMDA antagonists MK-801 and ketamine, confirming glutamate-induced excitotoxicity as a possible cause of neuronal degeneration in this mutant strain of rat.

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“…Additionally, these compounds differ in their binding site. MK-801 binds to the PCP site inside the pore of the receptor (Moring et al 1994; Sakurada et al 1993), whereas memantine is believed to bind at or near the Mg2+ binding site (Chen and Lipton 1997; Chen et al 1992). …”

Section: Methodsmentioning

confidence: 99%

Retrieval-induced NMDA receptor-dependent Arc expression in two models of cocaine-cue memory

Alaghband

O’Dell

Azarnia

et al. 2014

Neurobiology of Learning and Memory

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The association of environmental cues with drugs of abuse results in persistent drug-cue memories. These memories contribute significantly to relapse among addicts. While conditioned place preference (CPP) is a well-established paradigm frequently used to examine the modulation of drug-cue memories, very few studies have used the non-preference-based model conditioned activity (CA) for this purpose. Here, we used both experimental approaches to investigate the neural substrates of cocaine-cue memories. First, we directly compared, in a consistent setting, the involvement of cortical and subcortical brain regions in cocaine-cue memory retrieval by quantifying activity-regulated cytoskeletal associated gene (Arc) protein expression in both the CPP and CA models. Second, because NMDA receptor activation is required for Arc expression, we investigated the NMDA receptor dependency of memory persistence using the CA model. In both the CPP and CA models, drug-paired animals showed significant increases in Arc immunoreactivity in regions of the frontal cortex and amygdala compared to unpaired controls. Additionally, administration of a NMDA receptor antagonist (MK-801 or memantine) immediately after cocaine-CA memory reactivation impaired the subsequent conditioned locomotion associated with the cocaine-paired environment. The enhanced Arc expression evident in a subset of corticolimbic regions after retrieval of a cocaine-context memory, observed in both the CPP and CA paradigms, likely signifies that these regions: (i) are activated during retrieval of these memories irrespective of preference-based decisions, and (ii) undergo neuroplasticity in order to update information about cues previously associated with cocaine. This study also establishes the involvement of NMDA receptors in maintaining memories established using the CA model, a characteristic previously demonstrated using CPP. Overall, these results demonstrate the utility of the CA model for studies of cocaine-context memory and suggest the involvement of an NMDA receptor-dependent Arc induction pathway in drug-cue memory interference.

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Interaction of the NMDA receptor noncompetitive antagonist MK-801 with model and native membranes

Cited by 15 publications

References 44 publications

Common influences of non-competitive NMDA receptor antagonists on the consolidation and reconsolidation of cocaine-cue memory

Common influences of non-competitive NMDA receptor antagonists on the consolidation and reconsolidation of cocaine-cue memory

Effect of the Noncompetitive NMDA Antagonists MK-801 and Ketamine on the <i>Spastic</i> Han-Wistar Mutant: A Rat Model of Excitotoxicity

Retrieval-induced NMDA receptor-dependent Arc expression in two models of cocaine-cue memory

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