Sleep deprivation induces spatial memory impairment by altered hippocampus neuroinflammatory responses and glial cells activation in rats

Wadhwa, Meetu; Kumari, Pooja; Chauhan, Garima; Roy, Koustav; Alam, Shahid; Kishore, Krishna; Ray, Koushik; Panjwani, Usha

doi:10.1016/j.jneuroim.2017.09.003

Cited by 61 publications

(55 citation statements)

References 37 publications

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“…Animal models show that sleep loss associates with measures of neuroinflammation, such as increased secretion of pro‐inflammatory cytokines (Fernandes, Araujo, Tufik, & Andersen, ), increased blood–brain barrier permeability (Hurtado‐Alvarado et al., ) and activation of microglia (Wisor, Schmidt, & Clegern, ). Animal models also suggest that perturbations of microglial function lead to abnormal maturation of several brain cellular processes, including altered synaptogenesis, synaptic pruning, axonal growth and myelination, which result in behavioural abnormalities that emerge during the juvenile period (Johnson & Kaffman, ) and that imbalance of inflammatory cytokines in both hippocampus and plasma could mediate the detrimental effect of sleep restriction on memory (Wadhwa et al., ).…”

Section: What Are the Perspectives?mentioning

confidence: 99%

Perspectives in affective disorders: Clocks and sleep

Wirz‐Justice

Benedetti

2019

Eur J of Neuroscience

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Mood disorders are often characterised by alterations in circadian rhythms, sleep disturbances and seasonal exacerbation. Conversely, chronobiological treatments utilise zeitgebers for circadian rhythms such as light to improve mood and stabilise sleep, and manipulations of sleep timing and duration as rapid antidepressant modalities. Although sleep deprivation (“wake therapy”) can act within hours, and its mood‐elevating effects be maintained by regular morning light administration/medication/earlier sleep, it has not entered the regular guidelines for treating affective disorders as a first‐line treatment. The hindrances to using chronotherapeutics may lie in their lack of patentability, few sponsors to carry out large multi‐centre trials, non‐reimbursement by medical insurance and their perceived difficulty or exotic “alternative” nature. Future use can be promoted by new technology (single‐sample phase measurements, phone apps, movement and sleep trackers) that provides ambulatory documentation over long periods and feedback to therapist and patient. Light combinations with cognitive behavioural therapy and sleep hygiene practice may speed up and also maintain response. The urgent need for new antidepressants should hopefully lead to reconsideration and implementation of these non‐pharmacological methods, as well as further clinical trials. We review the putative neurochemical mechanisms underlying the antidepressant effect of sleep deprivation and light therapy, and current knowledge linking clocks and sleep with affective disorders: neurotransmitter switching, stress and cortico‐limbic reactivity, clock genes, cortical neuroplasticity, connectomics and neuroinflammation. Despite the complexity of multi‐system mechanisms, more insight will lead to fine tuning and better application of circadian and sleep‐related treatments of depression.

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Section: What Are the Perspectives?mentioning

confidence: 99%

Perspectives in affective disorders: Clocks and sleep

Wirz‐Justice

Benedetti

2019

Eur J of Neuroscience

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“…40 Both hippocampal-dependent memory impairment and hippocampal neuroinflammation, as evidenced by pro-inflammatory cytokine IL-6 levels and microglial activation, were present 24 h after sleep deprivation and this state persisted for seven days after sleep deprivation. In a separate study, 41 sleep deprivation was associated with increased levels of systemic and hippocampal TNF-α, IL-1β, IL-6 and IL-8 as well as decreased hippocampal and systemic levels of anti-inflammatory cytokines (IL-4; IL-10). Vacas et al explored the effects of 24-h pre-surgery sleep fragmentation in mice.…”

Section: Nutritionmentioning

confidence: 90%

Neuroinflammation is a putative target for the prevention and treatment of perioperative neurocognitive disorders

Saxena

Lai

et al. 2019

British Medical Bulletin

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Introduction: The demographics of aging of the surgical population has increased the risk for perioperative neurocognitive disorders in which trauma-induced neuroinflammation plays a pivotal role. Sources of data: After determining the scope of the review, the authors used PubMed with select phrases encompassing the words in the scope. Both preclinical and clinical reports were considered. Areas of agreement: Neuroinflammation is a sine qua non for development of perioperative neurocognitive disorders. Areas of controversy: What is the best method for ameliorating traumainduced neuroinflammation while preserving inflammation-based wound healing. Growing points: This review considers how to prepare for and manage the vulnerable elderly surgical patient through the entire spectrum, from preoperative assessment to postoperative period. Areas timely for developing research: What are the most effective and safest interventions for preventing and/or reversing Perioperative Neurocognitive Disorders.

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“…Neuroinflammation caused by sleep deprivation is associated with synaptic impairment, especially in the hippocampal area which is particularly sensitive to its detrimental effects [6,22]. To examine the effects of SS31 on inflammation in the hippocampus, we measured levels of three inflammatory cytokines-MCP-1, TNF-ɑ, and IL-6.…”

Section: Regulatory Proteins For Synaptic Plasticity Were Restored Amentioning

confidence: 99%

“…Cytokines such as TNF-α and IL-6 have been shown to induce changes in hippocampal dependent learning and memory tasks [23]. Increased hippocampal inflammation in relation to sleep deprivation has been well studied, and the effect of neuroinflammation on cognitive function can be detrimental [6,13,24]. SD mice treated with SS31 had a significant decrease in hippocampal inflammation, to a level similar to non-SD mice, suggesting that mitochondrial dysfunction appears to be related to the increased inflammation caused by short-term sleep deprivation in aging mice.…”

Section: Regulatory Proteins For Synaptic Plasticity Were Restored Amentioning

confidence: 99%

Adverse neurological effects of short-term sleep deprivation in aging mice are prevented by SS31 peptide

Dou

Ladiges

2020

Preprint

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Sleep deprivation is a potent stress factor that disrupts regulatory pathways in the brain resulting in cognitive dysfunction and increased risk of neurodegenerative disease with increasing age. Prevention of the adverse effects of sleep deprivation could be beneficial in older individuals by restoring healthy brain function. We report here on the ability of SS31, a mitochondrial specific peptide, to attenuate the negative neurological effects of short-term sleep deprivation in aging mice. C57BL/6 female mice, 20 months old, were subcutaneously injected with SS31 (3mg/kg) or saline daily for 4 days. Sleep deprivation was 4 hours daily for the last 2 days of SS31 treatment. Mice were immediately tested for learning ability followed by collection of brain and other tissues. In sleep deprived mice treated with SS31, learning impairment was prevented, brain mitochondrial ATP levels and synaptic plasticity regulatory proteins were restored, and ROS and inflammatory cytokines levels were decreased in the hippocampus. The observations suggest possible therapeutic benefits of SS31 for alleviating adverse neurological effects of acute sleep loss.

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Sleep deprivation induces spatial memory impairment by altered hippocampus neuroinflammatory responses and glial cells activation in rats

Cited by 61 publications

References 37 publications

Perspectives in affective disorders: Clocks and sleep

Perspectives in affective disorders: Clocks and sleep

Neuroinflammation is a putative target for the prevention and treatment of perioperative neurocognitive disorders

Adverse neurological effects of short-term sleep deprivation in aging mice are prevented by SS31 peptide

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