Acute sleep deprivation enhances avoidance learning and spatial memory and induces delayed alterations in neurochemical expression of GR, TH, DRD1, pCREB and Ki67 in rats

Azogu, Idu; Tremblaye, Patricia B. de la; Dunbar, Megan; Lebreton, M; LeMarec, Nathalie; Plamondon, Hélène

doi:10.1016/j.bbr.2014.11.015

Cited by 23 publications

(16 citation statements)

References 77 publications

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“…The contradictory result is interesting, however, in light of the antidepressant effects of sleep deprivation [22–24]. Additionally, there are studies that report enhanced memory formation and memory retrieval following brief periods of TSD [20,21]. This suggests that sleep deprivation can have different consequences across different settings and subjects.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, there seems to be some overlap between the brain regions affected by sleep loss and the brain regions known to be dysfunctional in depressive phenotypes, such as the medial prefrontal cortex and the hippocampus [15–19]. However, sleep deprivation can also have antidepressant effects in some patients, and has been shown to improve cognitive abilities in some cases [20–24]. The relationship between sleep loss and depression-related cognitive deficits is, therefore, still relatively obscure.…”

Section: Introductionmentioning

confidence: 99%

“…Animal investigations of depression-related cognitive deficits have applied tasks involving aversive or reinforcing stimuli, but, in humans, depressed patients show altered processing of punishment and reward cues [20,25–29]. Therefore, these tasks could report learning and memory deficits that are actually due to altered punishment and reward processing.…”

Section: Introductionmentioning

confidence: 99%

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Beyond Emotional and Spatial Processes: Cognitive Dysfunction in a Depressive Phenotype Produced by Long Photoperiod Exposure

2017

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Cognitive dysfunction in depression has recently been given more attention and legitimacy as a core symptom of the disorder. However, animal investigations of depression-related cognitive deficits have generally focused on emotional or spatial memory processing. Additionally, the relationship between the cognitive and affective disturbances that are present in depression remains obscure. Interestingly, sleep disruption is one aspect of depression that can be related both to cognition and affect, and may serve as a link between the two. Previous studies have correlated sleep disruption with negative mood and impaired cognition. The present study investigated whether a long photoperiod-induced depressive phenotype showed cognitive deficits, as measured by novel object recognition, and displayed a cognitive vulnerability to an acute period of total sleep deprivation. Adult male Wistar rats were subjected to a long photoperiod (21L:3D) or a normal photoperiod (12L:12D) condition. Our results indicate that our long photoperiod exposed animals showed behaviors in the forced swim test consistent with a depressive phenotype, and showed significant deficits in novel object recognition. Three hours of total sleep deprivation, however, did not significantly change novel object recognition in either group, but the trends suggest that the long photoperiod and normal photoperiod groups had different cognitive responses to total sleep deprivation. Collectively, these results underline the extent of cognitive dysfunction present in depression, and suggest that altered sleep plays a role in generating both the affective and cognitive symptoms of depression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Beyond Emotional and Spatial Processes: Cognitive Dysfunction in a Depressive Phenotype Produced by Long Photoperiod Exposure

2017

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“…Since depressive symptoms include anhedonia and despair, dopaminergic modulation of brain regions, which are part of the “reward system,” is particularly affected [ 33 – 35 ]. Animal studies have shown that exposure to ELA as well as variations in maternal care interferes with the maturation of catecholaminergic innervation and dopaminergic function in prefronto-limbic circuits [ 36 – 42 ] and induces sex-specific changes in dopamine receptor D1 (DRD1) density [ 43 ] as well as epigenetic modifications regulating the expression of the DRD1 receptor [ 44 , 45 ]. A key downstream regulator of dopaminergic signaling and mediator of actions and interactions of dopamine with other neurotransmitters is DARPP-32 (32-kDa dopamine- and cAMP-regulated phosphoprotein), which is phosphorylated upon activation of DRD1 receptors.…”

Section: Introductionmentioning

confidence: 99%

Early-Life Adversity Induces Epigenetically Regulated Changes in Hippocampal Dopaminergic Molecular Pathways

et al. 2018

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Early-life adversity (ELA) represents a major risk factor for the development of behavioral dysfunctions and mental disorders later in life. On the other hand, dependent on type, time point, and duration, ELA exposure can also induce adaptations, which result in better stress coping and resilience later in life. Guided by the hypothesis that chronic exposure to ELA results in dysfunctional brain and behavior, whereas short exposure to ELA may result in resilience, the behavioral and neurobiological consequences of long-term separation stress (LTSS) and short-term separation stress (STSS) were compared in a mouse model for ELA. In line with our hypothesis, we found that LTSS induced depressive-like behavior, whereas STSS reduced depressive-like behavioral symptoms. We then tested the hypothesis that the opposite behavioral outcomes of the two stress paradigms may be mediated by functional, epigenetically regulated changes of dopaminergic modulation in the hippocampal formation. We found that STSS exposure elevated dopamine receptor D1 (DRD1) gene expression and decreased gene expression of its downstream modulator DARPP-32 (32-kDa dopamine- and cAMP-regulated phosphoprotein), which was paralleled by decreased H3 acetylation at its gene promoter region. In contrast, LTSS elevated DARPP-32 gene expression, which was not paralleled by changes in histone acetylation and DRD1 gene expression. These findings indicate that short- and long-term neonatal exposure to ELA induces changes in dopaminergic molecular pathways, some of which are epigenetically regulated and which either alleviate or aggravate depressive-like symptoms later in life.

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“…Pharmacologic drugs targeting to the dopaminergic neurotransmission are clinically used for the treatment of many neuropsychiatric diseases [ 8 ]. Acute sleep deprivation elevated TH expression in the ventral tegmental area, nucleus accumbens, and hypothalamus [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine Ameliorates Sleep Deprivation-Induced Depressive Behaviors in Mice

Moon

Kim

et al. 2018

Int Neurourol J

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PurposeSleep deprivation induces depressive symptoms. Dexmedetomidine is a α2-adrenoreceptor agonist and this drug possesses sedative, anxiolytic, analgesic, and anesthetic-sparing effect. In this study, the action of dexmedetomidine on sleep deprivation-induced depressive behaviors was investigated using mice.MethodsFor the inducing of sleep deprivation, the mice were placed inside a water cage containing 15 platforms and filled with water up to 1 cm below the platform surface for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (0.5, 1, and 2 μg/kg) was intraperitoneally treated into the mice, one time per a day during 6 days. Then, forced swimming test and tail suspension test were conducted. Immunohistochemistry for tyrosine hydroxylase (TH), 5-hydroxytryptamine (5-HT; serotonin), tryptophan hydroxylase (TPH) and western blot for D1 dopamine receptor were also performed.ResultsSleep deprivation increased the immobility latency in the forced swimming test and tail suspension test. The expressions of TPH, 5-HT, and D1 dopamine receptor were decreased, whereas, TH expression was increased by sleep deprivation. Dexmedetomidine decreased the immobility latency and increased the expressions of TPH, 5-HT, and D1 dopamine receptor, whereas, HT expression was decreased by dexmedetomidine treatment.ConclusionsIn our results, dexmedetomidine alleviated sleep deprivation-induced depressive behaviors by increasing 5-HT synthesis and by decreasing dopamine production with up-regulation of D1 dopamine receptor.

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Acute sleep deprivation enhances avoidance learning and spatial memory and induces delayed alterations in neurochemical expression of GR, TH, DRD1, pCREB and Ki67 in rats

Cited by 23 publications

References 77 publications

Beyond Emotional and Spatial Processes: Cognitive Dysfunction in a Depressive Phenotype Produced by Long Photoperiod Exposure

Beyond Emotional and Spatial Processes: Cognitive Dysfunction in a Depressive Phenotype Produced by Long Photoperiod Exposure

Early-Life Adversity Induces Epigenetically Regulated Changes in Hippocampal Dopaminergic Molecular Pathways

Dexmedetomidine Ameliorates Sleep Deprivation-Induced Depressive Behaviors in Mice

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