Deficit of NMDA receptor activation in CA1 hippocampal area of aged rats is rescued by <scp>d</scp>‐cycloserine

Jm, Billard; Rouaud, Emilie

doi:10.1111/j.1460-9568.2007.05488.x

Cited by 87 publications

(69 citation statements)

References 59 publications

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“…In the current study, participants who received DCS showed greater potentiation of the VEP following HFvS compared with participants who received placebo. This is consistent with prior findings that DCS augmented increases in motor cortex excitability following anodal transcranial direct-current stimulation in humans (37) and augmented LTP in rat hippocampus following high-frequency electrical stimulation (38,39). Our finding is also consistent with preclinical studies demonstrating that potentiation of the VEP following HFvS is NMDAR dependent (8).…”

Section: Discussionsupporting

confidence: 82%

Augmenting NMDA receptor signaling boosts experience-dependent neuroplasticity in the adult human brain

Forsyth

Bachman

Mathalon

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Experience-dependent plasticity is a fundamental property of the brain. It is critical for everyday function, is impaired in a range of neurological and psychiatric disorders, and frequently depends on long-term potentiation (LTP). Preclinical studies suggest that augmenting N-methyl-D-aspartate receptor (NMDAR) signaling may promote experience-dependent plasticity; however, a lack of noninvasive methods has limited our ability to test this idea in humans until recently. We examined the effects of enhancing NMDAR signaling using D-cycloserine (DCS) on a recently developed LTP EEG paradigm that uses high-frequency visual stimulation (HFvS) to induce neural potentiation in visual cortex neurons, as well as on three cognitive tasks: a weather prediction task (WPT), an information integration task (IIT), and a n-back task. The WPT and IIT are learning tasks that require practice with feedback to reach optimal performance. The n-back assesses working memory. Healthy adults were randomized to receive DCS (100 mg; n = 32) or placebo (n = 33); groups were similar in IQ and demographic characteristics. Participants who received DCS showed enhanced potentiation of neural responses following repetitive HFvS, as well as enhanced performance on the WPT and IIT. Groups did not differ on the n-back. Augmenting NMDAR signaling using DCS therefore enhanced activitydependent plasticity in human adults, as demonstrated by lasting enhancement of neural potentiation following repetitive HFvS and accelerated acquisition of two learning tasks. Results highlight the utility of considering cellular mechanisms underlying distinct cognitive functions when investigating potential cognitive enhancers.D-cycloserine | NMDA receptor | neuroplasticity | long-term potentiation | learning E xperience-dependent neuroplasticity is the capacity of the brain to change in response to environmental input, learning, and use. It is a fundamental property of the brain and is critical for everyday functioning. It allows us to learn and remember patterns, predict and obtain reward, and refine and accelerate response selection for adaptive behavior (1). During development, experience-dependent plasticity interacts with genetic programming to organize neurons into the structurally and functionally connected circuits that characterize a mature brain. Although this basic circuitry is established by early adulthood, experience-dependent plasticity continues to shape connectivity within these circuits such that important inputs and action outputs are represented by larger and more coordinated populations of neurons. Given that these changes are the primary means through which the adult brain enables new behavior and that such plasticity is impaired in a range of neurological and psychiatric disorders (2), identifying manipulations that can harness experiencedependent plasticity offers exciting possibilities. Here, we tested whether augmenting N-methyl-D-aspartate receptor (NMDAR) activity could enhance experience-dependent plasticity in the adult human brain.The ...

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Section: Discussionsupporting

confidence: 82%

Augmenting NMDA receptor signaling boosts experience-dependent neuroplasticity in the adult human brain

Forsyth

Bachman

Mathalon

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…Because levels of basal excitatory synaptic transmission are normal in NCAM Ϫ/Ϫ mice, it is unlikely that a GluN2B-mediated increase in the basal activity of p38 MAPK (Kochlamazashvili et al, 2010) could depress basal transmission such that LTD would be occluded. Therefore, the impaired LTD in NCAM Ϫ/Ϫ mice is most likely due to a deficit in signaling via GluN2A-containing receptors, which is restored by DCS, as also has been reported for aged rats (Billard and Rouaud, 2007). In contrast, application of DCS in NCAM ϩ/ϩ mice increased GluN signaling to levels above the threshold for LTD induction, thus impairing LTD induction.…”

Section: Discussionsupporting

confidence: 61%

“…DCS is known to rescue deficits in GluN-dependent LTP in 23-to 27-month-old wild-type rats (Billard and Rouaud, 2007) and injured mice (Yaka et al, 2007). Two-way ANOVA of LTP levels in untreated and DCS-treated NCAM ϩ/ϩ and NCAM Ϫ/Ϫ mice revealed significant effects of genotype ( p ϭ 0.006) and DCS ( p ϭ 0.003) and a significant interaction between genotype and DCS ( p ϭ 0.002).…”

Section: Glun-but Not L-vdcc-dependent Ltp Is Impaired In Ncammentioning

confidence: 99%

Restoration of Synaptic Plasticity and Learning in Young and Aged NCAM-Deficient Mice by Enhancing Neurotransmission Mediated by GluN2A-Containing NMDA Receptors

Kochlamazashvili¹,

Bukalo²,

Senkov³

et al. 2012

J. Neurosci.

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Neural cell adhesion molecule (NCAM) is the predominant carrier of the unusual glycan polysialic acid (PSA)., but not NCAM ϩ/ϩ mice, there was a decline in LTP compared with 3-month-old mice that could be rescued by DCS. In 24-month-old mice of both genotypes, there was a reduction in LTP that could be fully restored by DCS in NCAM ϩ/ϩ mice but only partially restored in NCAM Ϫ/Ϫ mice. Thus, several deficiencies of NCAM Ϫ/Ϫ mice can be ameliorated by enhancing GluN2A-mediated neurotransmission with DCS.

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“…Glutamatergic activity and NMDA receptor density in the basal ganglia increase in patients with PD (23). Cycloserine is able to pass blood-brain barrier and enter the brain tissue where it acts as a partial agonist by binding to the binding site of the NMDA receptor (9). The effects of cycloserine on MPTP-induce motor disturbance may be related to increased neurotransmitter release and function in several inter-related cortical and subcortical systems.…”

Section: Discussionmentioning

confidence: 99%

“…Cycloserine, an anti-tuberculosis antibiotic, is a partial agonist of the glycine binding site of the N-methyl-D-aspartate (NMDA) receptor which improves object recognition in MPTP-lesioned monkeys (8), spatial navigation and learning deficits in aged rats (9,10) and anxiety-like behavior in rats (11,12).…”

Section: Introductionmentioning

confidence: 99%

Investigation of the Effect of Cycloserine on Motor Function in a Rat Model of Parkinson’s disease

Taherian

Arabahmadi

Taherian

2017

Caspian.J.Neurol.Sci

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Background:Previous studies have shown cycloserine to be neuroprotective in some neurodegenerative disorders. Objectives:To investigate the effect of cycloserine on motor function in Parkinson's disease in a rat model. Materials and Methods:Fifty-six healthy male wistar rats were used in this study and were divided into seven groups according to receiving saline, low dose (i.e. 100 mg/kg) and high dose (i.e. 200 mg/kg) of cycloserine for a short period (i.e. 8 days) (groups A-C, respectively) or long period (i.e. 16 days) (groups D-F, respectively) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-rat model of Parkinson. Also, a healthy group not receiving MPTP or any other drug was considered as the control group (group G). Apomorphine-induced rotational test (AIRT), elevated body swing test (EBST) and rotarod performance test (RPT) were done to examine behavioral performances.Results: Long-period treatment with cycloserine reduced MPTP-induced behavioral disturbances, i.e. net number of rotations in AIRT, net biased swing in EBST and reduced rotarod performance time in RPT, more than short period treatment. Although high dose of cycloserine was more effective than its low dose in reducing motor disturbance in initial trials of each test, long period treatment with low dose of cycloserine was similar to long period treatment with a high dose of it in reducing MPTP-induced Parkinsonism in EBST and RPT in latent trials. Conclusion:Long-period treatment with low-dose cycloserine seems to be the best option to obtain a sufficient neuroprotective effect for lowering motor disturbance in Parkinson's disease.

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Deficit of NMDA receptor activation in CA1 hippocampal area of aged rats is rescued by d‐cycloserine

Cited by 87 publications

References 59 publications

Augmenting NMDA receptor signaling boosts experience-dependent neuroplasticity in the adult human brain

Augmenting NMDA receptor signaling boosts experience-dependent neuroplasticity in the adult human brain

Restoration of Synaptic Plasticity and Learning in Young and Aged NCAM-Deficient Mice by Enhancing Neurotransmission Mediated by GluN2A-Containing NMDA Receptors

Investigation of the Effect of Cycloserine on Motor Function in a Rat Model of Parkinson’s disease

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