Regular ArticleDisseminated Corticolimbic Neuronal Degeneration Induced in Rat Brain by MK-801: Potential Relevance to Alzheimer's Disease☆
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2017, Frontiers in NeuroendocrinologyCitation Excerpt :Likewise, conflicting findings from postmortem studies has led to debate over whether gray matter loss reflects cell death or reduced neuropil and cell size (Schnieder and Dwork, 2011; Harrison, 1999). Animal studies employing NMDAR antagonists in both male and female rodents have had similarly inconclusive results, with some studies finding evidence of excitotoxicity and cell death (Ellison, 1994; Ellison and Switzer, 1993; Corso et al., 1997; Farber et al., 1995), and others finding cellular damage but no evidence of cell death (Genius et al., 2013; Wozniak et al., 1998). The conflicting results may stem from differences in dosage, length of treatment with NMDAR antagonists, and the length of recovery before analysis.
The NMDA receptor may participate in widespread suppression of circuit level neural activity, in addition to a similarly prominent role in circuit level activation
2012, Behavioural Brain ResearchCitation Excerpt :The neuronal damage produced by NMDAR antagonists in the rat can be prevented by cholinergic or GABAergic drugs known to suppress the psychotomimetic properties of ketamine [43]. MK-801 triggered widespread neuronal damage in the rat brain, where females showed more damage than males [44]. The above studies indicate that either activation of the NMDAR with agonists such as NMDA [3,4], or deactivation of the receptor with antagonist drugs [41–44], can produce neurotoxicity.
Memantine prevents aluminum-induced cognitive deficit in rats
2011, Behavioural Brain ResearchCitation Excerpt :The blockade of NMDA receptor-mediated excitotoxicity can help preserve neuronal structure and function [64–66]. The most significant problem being that at doses that exerted neuroprotective effects, NMDA antagonists caused adverse side effects ranging from memory dysfunction and psychotic reactions in humans [67–69] to acute injury and/or death of neurons in animal brain [70–72]. Memantine is rapidly displaced from the NMDA receptor, which may avoid prolonged receptor blockade and the detrimental effects on learning and memory associated with prolonged blockade of the NMDA receptor [64].
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L. HeimerN. Robards
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