Altered NMDA receptor trafficking contributes to sleep deprivation-induced hippocampal synaptic and cognitive impairments

Chen, Chu; Hardy, Marcia; Zhang, Jian; LaHoste, Gerald J.; Bazán, Nicolás G.

doi:10.1016/j.bbrc.2005.12.021

Cited by 94 publications

(70 citation statements)

References 33 publications

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“…The same research group also observed a higher proportion of NR1 and NR2A subunits of the NMDA receptor located intracellularly compared to surface level after sleep deprivation (McDermott et al 2006). This disruption in NMDA receptor trafficking to the cell surface and reduction in NMDA receptor-mediated current was also observed with 24 h of sleep deprivation (Chen et al 2006). Other groups have also observed decreases in NR1 protein expression in the hippocampus after sleep deprivation, supporting the hypothesis that the NMDA receptor is an important molecular target for sleep deprivation (Ravassard et al 2009;Chang et al 2012).…”

Section: N-methyl-d-aspartate (Nmda) Receptor and A-amino-3-hydroxy-5supporting

confidence: 53%

“…Other groups have also observed decreases in NR1 protein expression in the hippocampus after sleep deprivation, supporting the hypothesis that the NMDA receptor is an important molecular target for sleep deprivation (Ravassard et al 2009;Chang et al 2012). NR1 subunit decrease was accompanied by synaptic plasticity and memory deficits that could be rescued with pharmacological treatment of glycine, an NR1 agonist (McDermott et al 2003;Chen et al 2006). The NR2B subunit of the NMDA receptor has also been observed to decrease in the hippocampus as a result of REM sleep deprivation (Lopez et al 2008;Park et al 2012).…”

Section: N-methyl-d-aspartate (Nmda) Receptor and A-amino-3-hydroxy-5mentioning

confidence: 99%

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The impact of sleep loss on hippocampal function

2013

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Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values "work around the clock." Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs.

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Section: N-methyl-d-aspartate (Nmda) Receptor and A-amino-3-hydroxy-5supporting

confidence: 53%

Section: N-methyl-d-aspartate (Nmda) Receptor and A-amino-3-hydroxy-5mentioning

confidence: 99%

The impact of sleep loss on hippocampal function

2013

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“…When comparing control animals and those that were sleep-deprived for 24 hours, Chen et al (49) were unable to demonstrate a signifi cant difference in NR2Aor NR2B receptors. In addition, they found a signifi cant decrease in NMDA receptor-mediated excitatory postsynaptic potentials in hippocampal slices and hippocampus-mediated memory related to synaptic plasticity in the hippocampal NMDA receptors; their results were similar to ours.…”

Section: Discussionmentioning

confidence: 97%

“…The rats in the TSD group spent the entire 3 days of the experiment on a 3.3-cm platform (19). They were removed from the platform only during the test periods.…”

Section: Tsd Groupmentioning

confidence: 99%

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

Saygın¹,

Özgüner²,

Önder³

et al. 2017

BLL

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BACKGROUND: To examine the impact of different types of sleep deprivation on hippocampal-mediated learning and memory in rats. METHODS: Forty-eight Sprague-Dawley male rats were randomly assigned to 1 of 4 equal-size groups: (1) 12 hours of sleep per day (control). (2) total sleep deprivation (TSD), (3) rapid eye movement (REM) deprivation (RD), and (4) sleep restricted to 4 hours per day (SR). All rats were subjected to swimming training in the Morris water maze (MWM). At the end of the experiments, the rats were decapitated, and hippocampus tissue was analyzed for several neurotransmitters and receptors. RESULTS: The time spent at the target quadrant increased from 20.2 to 30.0 seconds in the control group on the third day of the experiment, whereas corresponding values increased from 20.2 to 21.8 seconds in the TSD group, 22.1 to 25.4 seconds in the RD group, and 21.2 to 32.0 sec in the SR group (p = 0.026). On the seventh day of the experiment, the values decreased to 25.0 seconds in controls, 22.5 in the RD group, and 23.6 in the SR group (p = 0.045). The TSD group demonstrated signifi cant decreases in glutamate and serotonin levels compared with the control group. There was a signifi cant increase in 5-HT2 a receptor expression in all intervention groups compared with the controls. CONCLUSIONS: Our results of glutamate levels and 5-HT2a receptor expression in the hippocampus seem to be primarily involved in sleep and memory regulation (Tab. 2, Fig. 4, Ref. 59). Text in PDF www.elis.sk.

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“…[63][64][65] In addition, of treatments with relatively rapid onset, ketamine hydrochloride exerts direct NMDAR antagonist effects, 47,63 and sleep deprivation induces internalization of NMDAR, reducing NMDAR function in hippocampal neurons. 66,67 Furey and Drevets Page 9Arch Gen Psychiatry. Author manuscript; available in PMC 2012 January 3.…”

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confidence: 99%

Antidepressant Efficacy of the Antimuscarinic Drug Scopolamine

Furey¹,

Drevets²

2006

Arch Gen Psychiatry

370

292

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Context-The need for improved therapeutic agents that more quickly and effectively treat depression is critical. In a pilot study we evaluated the role of the cholinergic system in cognitive symptoms of depression and unexpectedly observed rapid reductions in depression severity following the administration of the antimuscarinic drug scopolamine hydrobromide (4 μg/kg intravenously) compared with placebo (P=.002). Subsequently a clinical trial was designed to assess more specifically the antidepressant efficacy of scopolamine.Objective-To evaluate scopolamine as a potential antidepressant agent.Design-Two studies were conducted: a double-blind, placebo-controlled, dose-finding study followed by a double-blind, placebo-controlled, crossover clinical trial. Setting-The National Institute of Mental Health.Patients-Currently depressed outpatients aged 18 to 50 years meeting DSM-IV criteria for recurrent major depressive disorder or bipolar disorder. Of 39 eligible patients, 19 were randomized and 18 completed the trial.Interventions-Multiple sessions including intravenous infusions of placebo or scopolamine hydrobromide (4 μg/kg). Individuals were randomized to a placebo/ scopolamine or scopolamine/ placebo sequence (series of 3 placebo sessions and series of 3 scopolamine sessions). Sessions occurred 3 to 5 days apart.Main Outcome Measures-Psychiatric evaluations using the Montgomery-Asberg Depression Rating Scale and the Hamilton Anxiety Rating Scale were performed to assess antidepressant and antianxiety responses to scopolamine.Results-The placebo/scopolamine group showed no significant change during placebo infusion vs baseline; reductions in depression and anxiety rating scale scores (P<.001 for both) were observed after the administration of scopolamine compared with placebo. The scopolamine/ placebo group also showed reductions in depression and anxiety rating scale scores (P<.001 for both) after the administration of scopolamine, relative to baseline, and these effects persisted as they received placebo. In both groups, improvement was significant at the first evaluation after scopolamine administration (P≤.002).Conclusion-Rapid, robust antidepressant responses to the antimuscarinic scopolamine occurred in currently depressed patients who predominantly had poor prognoses.Correspondence: Maura L. Furey, PhD, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, 15K North Dr, Bldg 15K, Room 115B, Bethesda, MD 20892 (mfurey@mail.nih.gov). Additional Information: A use-patent application for the use of scopolamine as an antidepressant agent has been filed. NIH Public Access Author ManuscriptArch Gen Psychiatry. Author manuscript; available in PMC 2012 January 3. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptMajor depression is the leading cause of years lived with disability. 1 A range of antidepressant agents is available, but 30% to 40% of patients with major depressive disorder (MDD) do not respond to initial treatment, 2 an...

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Altered NMDA receptor trafficking contributes to sleep deprivation-induced hippocampal synaptic and cognitive impairments

Cited by 94 publications

References 33 publications

The impact of sleep loss on hippocampal function

The impact of sleep loss on hippocampal function

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

Antidepressant Efficacy of the Antimuscarinic Drug Scopolamine

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