Lithium Prevents REM Sleep Deprivation-Induced Impairments on Memory Consolidation

Ota, Simone Marie; Moreira, Karin Di Monteiro; Suchecki, Deborah; Oliveira, Maria Gabriela Menezes; Tiba, Paula Ayako

doi:10.5665/sleep.3126

Cited by 17 publications

(11 citation statements)

References 39 publications

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“…Li + may be able to alleviate the hyperarousal by downregulating the interaction between NCS-1 and InsP3, thus decreasing high-frequency activity. This theory is supported by evidence that Li + treatment has been seen to increase slow wave sleep and reduce REM sleep (Friston et al 1989;Zamboni et al 1999;Qureshi and Lee-Chiong 2004;Jones et al 2008;Ota et al 2013), as well as increase REM sleep latency (Campbell et al 1989). The downregulation by Li + of NCS-1 interactions with InsP3 reduces the abnormal high-frequency activity and restores proper rhythms to these systems.…”

Section: Discussionmentioning

confidence: 89%

Lithium decreases the effects of neuronal calcium sensor protein 1 in pedunculopontine neurons

et al. 2016

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Human postmortem studies reported increased expression of neuronal calcium sensor protein 1 (NCS‐1) in the brains of some bipolar disorder patients, and reduced or aberrant gamma band activity is present in the same disorder. Bipolar disorder is characterized by sleep dysregulation, suggesting a role for the reticular activating system (RAS). Lithium (Li+) has been shown to effectively treat the mood disturbances in bipolar disorder patients and was proposed to act by inhibiting the interaction between NCS‐1 and inositol 1,4,5‐triphosphate receptor protein (InsP3R). NCS‐1 is known to enhance the activity of InsP3R, and of Ca2+‐mediated gamma oscillatory activity in the pedunculopontine nucleus (PPN), part of the RAS. This study aimed to determine the nature of some of the intracellular mechanisms of Li+ on rat PPN cells and to identify the interaction between Li+ and NCS‐1. Since Li+ has been shown to act by inhibiting the enhancing effects of NCS‐1, we tested the hypothesis that Li+ would reduced the effects of overexpression of NCS‐1 and prevent the downregulation of gamma band activity. Li+ decreased gamma oscillation frequency and amplitude by downregulating Ca2+ channel activity, whereas NCS‐1 reduced the effect of Li+ on Ca2+ currents. These effects were mediated by a G‐protein overinhibition of Ca2+ currents. These results suggest that Li+ affected intracellular pathways involving the activation of voltage‐gated Ca2+ channels mediated by an intracellular mechanism involving voltage‐dependent activation of G proteins, thereby normalizing gamma band oscillations mediated by P/Q‐type calcium channels modulated by NCS‐1.

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Section: Discussionmentioning

confidence: 89%

Lithium decreases the effects of neuronal calcium sensor protein 1 in pedunculopontine neurons

et al. 2016

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“…Rather, it reflects the assumptions that SD-induced memory impairment is mainly attributed to an alteration of vigilance state quantities. According to the sequential hypothesis (SH), SD-induced memory deficits are based on changes in proportion among the different phases of sleep [53,54]. Parallel to these well-documented effects on cognitive functions, several neurotransmitters, cellular and molecular correlates of synaptic plasticity within the hippocampus of experimental animals have also been shown to be influenced by SD [15][16][17].…”

Section: Discussionmentioning

confidence: 98%

Ovariectomy does not exacerbate the negative effects of sleep deprivation on synaptic plasticity in rats

Hajali

Sheibani

Mahani

et al. 2015

Physiology & Behavior

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“…Rather, it replicates the assumptions that SD-induced memory impairment is primarily attributed to an alteration of vigilance state quantities. Accordingly, the sequential hypothesis (SH) claims that SD-induced memory deficits are based on altered proportion of different phases of sleep (Giuditta, 2014;Ota, Moreira, et al, 2013). In addition to these well-known effects on cognitive functions, several neurotransmitters, cellular and molecular factors involved in synaptic plasticity within the hippocampus of rodents have also been shown to be influenced by SD (Guzman-Marin et al, 2006;Longordo, Kopp, et al, 2009;Ravassard et al, 2009).…”

Section: Discussionmentioning

confidence: 98%

Effect of castration on the susceptibility of male rats to the sleep deprivation-induced impairment of behavioral and synaptic plasticity

Hajali

Sheibani

Ghazvini

et al. 2015

Neurobiology of Learning and Memory

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In both human and animal studies, the effect of sleep deficiency on cognitive performances has mostly been studied during adulthood in males, but very little data exist concerning the effects of poor sleep in gonadal hormones-depleted status, such as aging or gonadectomized (GDX) male animal models. The present study investigated the potential modulatory effects of the endogenous male sex hormones on the 48h REM sleep deprivation (SD)-induced cognitive and synaptic impairments by comparing the gonadally intact with castrated male rats, a rodent model of androgen-deprived male animals. The multiple platform method was used for inducing REM-SD and spatial performances were evaluated using Morris water maze (MWM) task. Early long-term potentiation (E-LTP) was measured in area CA1 of the hippocampus and PCR and western blotting assays were employed to assess brain derived neurotrophic factor (BDNF) gene and protein expression in the hippocampus. To reveal any influence of sleep loss on stress level, we also evaluated the plasma corticosterone levels of animals. Regardless of reproductive status, REM-SD significantly disrupted short-term memory and LTP, as well as hippocampal BDNF expression. The corticosterone levels were not significantly changed following REM-SD neither in intact nor in GDX male rats. These findings suggest that depletion of male sex steroid hormones by castration does not lead to any heightened sensitivity of male animals to the deleterious effects of 48h REM-SD on cognitive and synaptic performances.

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Lithium Prevents REM Sleep Deprivation-Induced Impairments on Memory Consolidation

Abstract: Lithium reduced rapid eye movement sleep and prevented memory impairment induced by sleep deprivation. These results indicate that these phenomena may be related, but cause-effect relationship cannot be ascertained.

Cited by 17 publications

References 39 publications

Lithium decreases the effects of neuronal calcium sensor protein 1 in pedunculopontine neurons

Lithium decreases the effects of neuronal calcium sensor protein 1 in pedunculopontine neurons

Ovariectomy does not exacerbate the negative effects of sleep deprivation on synaptic plasticity in rats

Effect of castration on the susceptibility of male rats to the sleep deprivation-induced impairment of behavioral and synaptic plasticity

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