Cognition-enhancing and anxiolytic effects of memantine

Minkeviciene, Rimante; Banerjee, Pradeep; Tanila, Heikki

doi:10.1016/j.neuropharm.2008.02.014

Cited by 51 publications

(35 citation statements)

References 21 publications

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“…Memantine pretreatment fully blocked compulsive eating, bringing the intake of the Palatable food group to the control Chow level. We can confidently exclude that the effect of drug treatment on the light/dark conflict test was influenced by a potential anxiogenic effect, as memantine has been shown to exert either no effect or anxiolytic effects (Koltunowska et al, 2013;Minkeviciene et al, 2008).…”

Section: Discussionmentioning

confidence: 98%

The Uncompetitive N-methyl-D-Aspartate Antagonist Memantine Reduces Binge-Like Eating, Food-Seeking Behavior, and Compulsive Eating: Role of the Nucleus Accumbens Shell

Smith

Rao

Velázquez-Sánchez

et al. 2014

Neuropsychopharmacol

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Binge-eating disorder is characterized by excessive, uncontrollable consumption of palatable food within brief periods of time. The role of the glutamatergic N-methyl-D-aspartate (NMDA) receptor system in hedonic feeding is poorly understood. The aim of this study was to characterize the effects of the uncompetitive NMDA receptor antagonist memantine on palatable food-induced behavioral adaptations using a rat model, which mimics the characteristic symptomatology observed in binge-eating disorder. For this purpose, we allowed male Wistar rats to respond to obtain a highly palatable, sugary diet (Palatable group) or a regular chow diet (Chow control group), for 1 h a day, under a fixed-ratio 1 (FR1) schedule of reinforcement. Upon stabilization of food responding, we tested the effects of memantine on the Chow and Palatable food groups' intake. Then, we tested the effects of memantine on food-seeking behavior, under a second-order schedule of reinforcement. Furthermore, we investigated the effects of memantine on the intake of food when it was offered in an aversive, bright compartment of a light/dark conflict test. Finally, we evaluated the effects of memantine on FR1 responding for food, when microinfused into the nucleus accumbens (NAcc) shell or core. Memantine dose-dependently decreased binge-like eating and fully blocked food-seeking behavior and compulsive eating, selectively in the Palatable food group. The drug treatment did not affect performance of the control Chow food group. Finally, intra-NAcc shell, but not core, microinfusion of memantine decreased binge-like eating. Together, these findings substantiate a role of memantine as a potential pharmacological treatment for binge-eating disorder.

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Section: Discussionmentioning

confidence: 98%

The Uncompetitive N-methyl-D-Aspartate Antagonist Memantine Reduces Binge-Like Eating, Food-Seeking Behavior, and Compulsive Eating: Role of the Nucleus Accumbens Shell

Smith

Rao

Velázquez-Sánchez

et al. 2014

Neuropsychopharmacol

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“…10 In this study, 6-, 9-and 15-month-old homozygous 3xTg-AD mice, 10 per group (five male, five female); littermates or cousins, and agematched NonTg mice were treated for 3 months with vehicle only (2% sucrose in water; littermates or cousins) or a clinically relevant dose of memantine (30 mg/kg/ day), shown to produce a steady-state plasma drug level of approximately 1 mol/L in mice. 23,26 In clinical practice, a stable dose of 20 mg/day memantine in patients with AD produces a steady-state plasma drug level of approximately 0.5 mol/L. 27,28 Memantine is known to block the NMDA receptors with an IC 50 of about 1 mol/L, and it blocks synaptic plasticity (eg, LTP) only at much higher concentrations (IC 50 ϭ 11.6 mol/L).…”

Section: Animals and Treatmentmentioning

confidence: 99%

Memantine Improves Cognition and Reduces Alzheimer’s-Like Neuropathology in Transgenic Mice

Martínez-Coria

Green

Billings

et al. 2010

The American Journal of Pathology

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194

110

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Memantine is an N-methyl-D-aspartate receptor antagonist that is approved for the treatment of moderate to severe Alzheimer's disease (AD). In this study, three groups of triple-transgenic (3xTg-AD) mice with differing levels of AD-like pathology (6, 9, and 15 months of age) were treated for 3 months with doses of memantine equivalent to those used in humans. After the treatment, memantine-treated mice had restored cognition and significantly reduced the levels of insoluble amyloid-␤ (A␤), A␤ dodecamers (A␤*56), prefibrillar soluble oligomers , and fibrillar oligomers. The effects on pathology were stronger in older, more impaired animals. Memantine treatment also was associated with a decline in the levels of total tau and hyperphosphorylated tau. Finally, memantine pre-incubation prevented A␤-induced inhibition of long-term potentiation in hippocampal slices of cognitively normal mice. These results suggest that the effects of memantine treatment on AD brain include disease modification and prevention of synaptic dysfunction.

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“…Whilst memantine may show signs of inducing cognitive disruption in normal animals and humans, a number of papers have reported positive effects in preclinical models of cognitive impairment, e.g. transgenic mice engineered to overexpress amyloid proteins and lesioned rats (Creeley et al 2006;Minkeviciene et al 2004Minkeviciene et al , 2008More et al 2008;Yuede et al 2007). Also, memantine appears to provide some clinical benefit to Alzheimer's patients (Witt et al 2004).…”

Section: Memantine and Nvp-aam077mentioning

confidence: 99%

A comparison of the effects of ketamine and phencyclidine with other antagonists of the NMDA receptor in rodent assays of attention and working memory

et al. 2011

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Overall, the opportunity to induce a selective cognitive deficit in attention (5CSRT) or working memory (DMTP) in the rat is limited by both the NMDAR antagonist and the dose range used. The importance of a preclinical focus on ketamine, which is used more frequently in clinical settings, is limited by the extent to which cognitive effects can be both detected and quantified using this exposure regimen within these two operant assays.

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Cognition-enhancing and anxiolytic effects of memantine

Cited by 51 publications

References 21 publications

The Uncompetitive N-methyl-D-Aspartate Antagonist Memantine Reduces Binge-Like Eating, Food-Seeking Behavior, and Compulsive Eating: Role of the Nucleus Accumbens Shell

The Uncompetitive N-methyl-D-Aspartate Antagonist Memantine Reduces Binge-Like Eating, Food-Seeking Behavior, and Compulsive Eating: Role of the Nucleus Accumbens Shell

Memantine Improves Cognition and Reduces Alzheimer’s-Like Neuropathology in Transgenic Mice

A comparison of the effects of ketamine and phencyclidine with other antagonists of the NMDA receptor in rodent assays of attention and working memory

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