NMDA receptor-mediated glutamate toxicity of cultured cerebellar, cortical and mesencephalic neurons: neuroprotective properties of amantadine and memantine

Weller, Michael; Finiels-Marlier, Françoise; Paul, Steven M.

doi:10.1016/0006-8993(93)90464-x

Cited by 70 publications

(38 citation statements)

References 28 publications

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“…In agreement with our previous work (Challiss et al, 1994b) (Challiss et al, 1994a) (Seif el Nasr et al, 1990;Erdo & Schaefer, 1991;Chen et al, 1992;Keilhoff & Wolf, 1992;Weller et al, 1993).…”

Section: Discussionsupporting

confidence: 93%

Modulation of NMDA effects on agonist‐stimulated phosphoinositide turnover by memantine in neonatal rat cerebral cortex

Mistry

Wilke

Challiss

1995

British J Pharmacology

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Section: Discussionsupporting

confidence: 93%

Modulation of NMDA effects on agonist‐stimulated phosphoinositide turnover by memantine in neonatal rat cerebral cortex

Mistry

Wilke

Challiss

1995

British J Pharmacology

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“…On the other hand, memantine is well known to act as an antagonist on Nmethyl-D-aspartic acid (NMDA) receptors and has a protective effect against neuronal damage induced by excess glutamic acid (6). Clinically, memantine is used for the treatment of moderate or severe AD, especially in developed regions, including the USA and Europe (7).…”

Section: Introductionmentioning

confidence: 99%

Characteristic Effects of Anti-dementia Drugs on Rat Sleep Patterns

Ishida

Kamei

2009

J Pharmacol Sci

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Abstract. The present study was undertaken to clarify the effects of anti-dementia drugs on sleep pattern in rats. Electrodes were chronically implanted into the frontal cortex and the dorsal neck muscle of rats for the electroencephalogram (EEG) and electromyogram (EMG), respectively. EEG and EMG were recorded with an electroencephalograph. SleepSigh ver. 2.0 was used for analysis of the sleep-wake state. Total times of waking, non-rapid eye movement (non-REM) sleep, and rapid eye movement (REM) sleep were measured from 10:30 to 16:30. Galantamine had no significant influence on the sleep pattern. On the other hand, donepezil and memantine showed significant increases in sleep latency and total waking time and a decrease in total non-REM sleep time. Furthermore, memantine decreased total REM sleep time. To investigate the characteristics of non-REM sleep in detail, non-REM sleep was classified as stage 1, 2, or 3 according to the depth of sleep. Different from donepezil and galantamine, memantine significantly decreased stage 1 and increased stage 3 in non-REM sleep. From these findings, it can be concluded that galantamine caused no sleep disturbance, different from donepezil and memantine.

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“…The rationale for using memantine in AD patients is based on the hypothesis that blockade of NMDA receptormediated excitotoxicity can help preserve neuronal structure and function (Lipton, 2006(Lipton, , 2007Wenk et al, 2006). The ability of memantine to protect neurons against NMDA-or glutamate-induced excitotoxicity has been shown in vitro (Erdö and Schäfer, 1991;Chen et al, 1992;Weller et al, 1993), and in animal models of neurodegenerative disease (Wenk et al, 1995(Wenk et al, , 1997(Wenk et al, , 2006MiguelHidalgo et al, 2002). Therefore, it has been proposed that memantine can improve cognition in AD and perhaps even slow disease progression by blocking NMDA receptormediated excitotoxicity (Ditzler, 1991;Frankiewicz et al, 2000;Reisberg et al, 2003;Lipton, 2006).…”

Section: Introductionmentioning

confidence: 99%

Effects of Memantine on Neuronal Structure and Conditioned Fear in the Tg2576 Mouse Model of Alzheimer's Disease

Dong

Yuede

Coughlan

et al. 2008

Neuropsychopharmacol

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Memantine, an uncompetitive NMDA receptor antagonist used for the treatment of Alzheimer's disease (AD), has been hypothesized to have neuroprotective properties. However, the similarity of its mechanism of action to other NMDA receptor antagonists has led to concerns that it may also have neurotoxic effects. To assess both the neuroprotective and neurotoxic potential of memantine in a mouse model of AD (Tg2576 mice), we used quantitative light and electron microscopy to investigate the effects of long-term (6 months) administration of memantine (5, 10 and 20 mg/kg) on plaque deposition and neuronal morphology in the hippocampus and overlying cortex. A fear-conditioning paradigm was used to evaluate the behavioral consequences of any observed changes in structure. Administration of the two higher doses of memantine (10 and 20 mg/kg) was associated with a significant decrease in b-amyloid (Ab) plaque deposition, increases in synaptic density and the appearance of degenerating axons; the latter two effects were independent of genotype. Administration of the lowest dose of memantine (5 mg/kg) was associated with a significant decrease in Ab plaque deposition and a significant increase in synaptic density, but not a significant increase in degenerating axons. However, memantine did not significantly improve behavioral deficits associated with genotype in a fear-conditioning paradigm at any dose. These results suggest that chronic memantine administration may have both neuroprotective and neurotoxic effects in a mouse model of AD.

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NMDA receptor-mediated glutamate toxicity of cultured cerebellar, cortical and mesencephalic neurons: neuroprotective properties of amantadine and memantine

Cited by 70 publications

References 28 publications

Modulation of NMDA effects on agonist‐stimulated phosphoinositide turnover by memantine in neonatal rat cerebral cortex

Modulation of NMDA effects on agonist‐stimulated phosphoinositide turnover by memantine in neonatal rat cerebral cortex

Characteristic Effects of Anti-dementia Drugs on Rat Sleep Patterns

Effects of Memantine on Neuronal Structure and Conditioned Fear in the Tg2576 Mouse Model of Alzheimer's Disease

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