Inhibited Endogenous H2S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment

Yang, San-Qiao; Jiang, Li; Lan, Fang; Wei, Hou; Xie, Ming; Zou, Wei; Zhang, Ping; Wang, Chunyan; Xie, Yurong; Tang, Xiao‐Qing

doi:10.3389/fpsyg.2019.00053

Cited by 24 publications

(12 citation statements)

References 70 publications

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“…LC3 (microtubule-associated protein light chain 3, MAP LC3) was the first autophagosome marker protein to be identified in mammals and is homologous to the yeast autophagy-related gene Atg8. Similar to previous studies, SD has been shown to cause excessive levels of autophagy and may be one of the causes of impairment of learning and memory (8,29,30).…”

Section: Discussionsupporting

confidence: 83%

Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy

Dai¹,

Xiao²,

Tu³

et al. 2021

Ann Transl Med

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Background: Sleep deprivation (SD) causes a disturbance in the cognitive function of rats. While propofol has a powerful sedative and hypnotic effect and is an antioxidant, its effect on the cognitive function of rats following SD remains unknown. The purpose of this study was to explore the protective effects of propofol on excessive autophagy and mitophagy in the hippocampus of rats after SD.Methods: Adult male rats were intraperitoneally injected with 30 mg/kg of propofol after 96 hours of SD.Then we evaluated the effect of propofol on the cognitive function of sleep deprived rats by the Morris water maze. Transmission electron microscopy, Western blotting, PCR, immunohistochemistry, autophagy enhancer and autophagy inhibitor were used to study the effect of propofol on hippocampal neurons of rat with excessive autophagy and mitophagy. Results:The behavioral experimental results of the Morris water maze showed that propofol improved the learning and memory ability of sleep-deprived rats. The expression of Beclin1, PINK1, parkin, p62, and LC3 protein increased significantly after sleep deprivation. While the intervention of propofol could significantly reduce the expression of these proteins, rapamycin treatment eliminated this effect.Conclusions: Our findings showed that propofol could reduce the impairment of learning and memory in sleep-deprived rats by inhibiting excessive autophagy and mitophagy in hippocampal neurons. This strategy may provide an application basis for the clinical use of propofol in patients with chronic insomnia.

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Section: Discussionsupporting

confidence: 83%

Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy

Dai¹,

Xiao²,

Tu³

et al. 2021

Ann Transl Med

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“…The Y-maze experiment was performed due to the animals’ nature of showing a preference to explore novel locations rather than going back to a previously explored arm ( Mo et al, 2013 ; Yang et al, 2019 ). In the Y-maze, the spontaneous test was performed to determine spatial working memory.…”

Section: Resultsmentioning

confidence: 99%

Long-Term Social Isolation-Induced Autophagy Inhibition and Cell Senescence Aggravate Cognitive Impairment in D(+)Galactose-Treated Male Mice

Wang

Ntim

Xia

et al. 2022

Front. Aging Neurosci.

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Aging is associated with physiological and pathological changes and presents health complications, such as dementia. Isolation has also been associated with the experience of growing old. Both have been linked individually to the incidence of cognitive decline. In this present study, the effects of these two phenomena have been looked at in animal models where aging was induced with D(+)Galactose in mice who underwent long-term post-weaned social isolation (L-PWSI). Assessing cognitive function using Y-maze, Morris water maze (MWM), and passive avoidance tests (PATs) confirmed that cognition is impaired in either of the treatments but worsened when the D(+)Galactose mice were subjected to L-PWSI. Moreover, a synaptic protein, PSD95, and dendritic spines density were significantly reduced in the L-PWSI and D(+)Galactose-treated mice. Our previous study revealed that autophagy deficit is involved in cognitive impairment in the L-PWSI model. Here, we first report the inhibited cell cycle in L-PWSI, combined with the decreased autophagy, aggravates cognitive impairment in D(+)Galactose-treated mice. Beyond these, the autophagy and cell cycle mechanisms that link isolation and aging have been explored. The close association between isolation and aging in humans is very real and needs much research attention going forward for possible therapeutic interventions.

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“…Different hypotheses have been suggested for the impairment effect of SD on memory performance. A previous study has shown that SD impairs the rats’ performance in several memory tests, due to the induction of autophagy in the hippocampus (Yang et al, 2019). In the radial arm maze, SD disrupts memory performance via attenuating hippocampal antioxidant capacity (Alzoubi et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Investigating the effect of crocin on memory deficits induced by total sleep deprivation (TSD) with respect to the BDNF, TrkB and ERK levels in the hippocampus of male Wistar rats

et al. 2021

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Background: Sleep deprivation (SD) induces cognitive impairments such as memory deficit. Brain-derived neurotrophic factor (BDNF) is considered as the most critical neurotrophin in the central nervous system that is involved in sleep and memory. The main receptor of BDNF, tropomyosin receptor kinase B (TrkB), is dramatically expressed in the hippocampus. Also, extracellular signal-regulated kinase (ERK) has a significant role in memory function. Crocin is a carotenoid chemical compound and the active component of the flower Crocus sativus L. (saffron) that improves memory function and increases the level of BDNF, TrkB and ERK. Aims: In this research, we aimed to investigate the effect of total SD (TSD, 24 h) and crocin on memory performance, and BDNF, TrkB and ERK hippocampal levels. Methods: Passive avoidance memory was assessed using step-through, and working memory was measured using Y-maze tasks. The level of proteins in both hemispheres of the hippocampus was evaluated using Western blotting. Crocin was injected intraperitoneally at doses of 1, 5 and 15 mg/kg. Results: Twenty-four-hour TSD impaired both types of memories and decreased the level of all proteins in both hemispheres of the hippocampus. Crocin at all doses restored TSD-induced memory deficits. Crocin (15 mg/kg) reversed the effect of TSD on levels of all proteins. Conclusions: The adverse effect of TSD on the level of proteins in the hippocampus may disrupt synaptic plasticity and transmission, which induces memory impairment. Additionally, the restoration effect of crocin on the decrease in protein levels may be involved in its improvement effect on memory performance.

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Inhibited Endogenous H2S Generation and Excessive Autophagy in Hippocampus Contribute to Sleep Deprivation-Induced Cognitive Impairment

Cited by 24 publications

References 70 publications

Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy

Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy

Long-Term Social Isolation-Induced Autophagy Inhibition and Cell Senescence Aggravate Cognitive Impairment in D(+)Galactose-Treated Male Mice

Investigating the effect of crocin on memory deficits induced by total sleep deprivation (TSD) with respect to the BDNF, TrkB and ERK levels in the hippocampus of male Wistar rats

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