scholarly journals Stem-leaf saponins from Panax notoginseng counteract aberrant autophagy and apoptosis in hippocampal neurons of mice with cognitive impairment induced by sleep deprivation

2020 ◽  
Vol 44 (3) ◽  
pp. 442-452 ◽  
Author(s):  
Yin Cao ◽  
Yingbo Yang ◽  
Hui Wu ◽  
Yi Lu ◽  
Shuang Wu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Sleep Deprivation ◽  
Hippocampal Neurons ◽  
Panax Notoginseng ◽  
Stem Leaf

scholarly journals Sleep Deprivation Aggravates Cognitive Impairment by the Alteration of Hippocampal Neuronal Activity and the Density of Dendritic Spine in Isoflurane-Exposed Mice

2020 ◽  
Vol 14 ◽  
Author(s):  
Kai Zhang ◽  
Naqi Lian ◽  
Ran Ding ◽  
Cunle Guo ◽  
Xi Dong ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Sleep Deprivation ◽  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Short Term Memory ◽  
Elective Surgery ◽  
Long Term Memory ◽  
General Anesthetic ◽  
Term Memory

Isoflurane contributes to cognitive deficits when used as a general anesthetic, and so does sleep deprivation (SD). Patients usually suffer from insomnia before an operation due to anxiety, fear, and other factors. It remains unclear whether preoperative SD exacerbates cognitive impairment induced by isoflurane. In this study, we observed the effects of pretreated 24-h SD in adult isoflurane-exposed mice on the cognitive behaviors, the Ca2+ signals of dorsal hippocampal CA1 (dCA1) neurons in vivo with fiber photometry, and the density of dendritic spines in hippocampal neurons. Our results showed that in cognitive behavior tasks, short-term memory damages were more severe with SD followed by isoflurane exposure than that with SD or isoflurane exposure separately, and interestingly, severe long-term memory deficits were induced only by SD followed by isoflurane exposure. Only the treatment of SD followed by isoflurane exposure could reversibly decrease the amplitude of Ca2+ signals when mice were freely moving and increase the duration of Ca2+ signals during the long-term memory behavior test. The density of dendritic spines with both SD and isoflurane exposure was lower than that with SD alone. This study suggests that SD should be avoided preoperatively in patients undergoing elective surgery under isoflurane anesthesia.

scholarly journals Notoginsenoside R1 Reverses Abnormal Autophagy in Hippocampal Neurons of Mice With Sleep Deprivation Through Melatonin Receptor 1A

2021 ◽  
Vol 12 ◽  
Author(s):  
Yin Cao ◽  
Qinglin Li ◽  
An Zhou ◽  
Zunji Ke ◽  
Shengqi Chen ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Signaling Pathway ◽  
Learning And Memory ◽  
Hippocampal Neurons ◽  
Panax Notoginseng ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Melatonin Receptor ◽  
Sleep Regulation ◽  
Neural Injury

Sleep deprivation (SD) may cause serious neural injury in the central nervous system, leading to impairment of learning and memory. Melatonin receptor 1A (MTNR1A) plays an important role in the sleep regulation upon activation by melatonin. The present study aimed to investigate if notoginsenoside R1 (NGR1), an active compound isolated from Panax notoginseng, could alleviate neural injury, thus improve impaired learning and memory of SD mice, as well as to explore its underlying action mechanism through modulating MTNR1A. Our results showed that NGR1 administration improved the impaired learning and memory of SD mice. NGR1 prevented the morphological damage and the accumulation of autophagosomes in the hippocampus of SD mice. At the molecular level, NGR1 reversed the expressions of proteins involved in autophagy and apoptosis, such as beclin-1, LC3B, p62, Bcl-2, Bax, and cleaved-caspase 3. Furthermore, the effect of NGR1 was found to be closely related with the MTNR1A-mediated PI3K/Akt/mTOR signaling pathway. On HT-22 cells induced by autophagy inducer rapamycin, NGR1 markedly attenuated excessive autophagy and apoptosis, and the alleviative effect was abolished by the MTNR1A inhibitor. Taken together, NGR1 was shown to alleviate the impaired learning and memory of SD mice, and its function might be exerted through reduction of excessive autophagy and apoptosis of hippocampal neurons by regulating the MTNR1A-mediated PI3K/Akt/mTOR signaling pathway.

Antagonism by modafinil of the psychomotor and cognitive impairment induced by sleep-deprivation in 12 healthy volunteers

1991 ◽  
Vol 6 (2) ◽  
pp. 93-97 ◽  
Author(s):  
G Bensimon ◽  
D Benoit ◽  
L Lacomblez ◽  
E Weiller ◽  
D Warot ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Sleep Deprivation ◽  
Healthy Volunteers ◽  
Controlled Study ◽  
Long Term Memory ◽  
Double Blind ◽  
Flicker Fusion Frequency ◽  
Short And Long Term ◽  
Psychotropic Compound

SummaryModafinil is a new psychotropic compound with central α1, adrenergic-stimulant activity in animals. In the present study, its pharmacological activity in man was evaluated in the sleep-deprivation induced psychomotor and cognitive impairment paradigm. This was a double-blind placebo-controlled study involving 12 healthy volunteers. Standard psychomotor and memory tasks were used, including critical flicker fusion frequency determination (CFF), choice reaction time and short- and long-term memory evaluation. Results revealed a clear antagonism by modafinil of the psychomotor and cognitive impairment induced by sleep-deprivation in most tasks 6 h after drug administration, and marginal effects 18 h after. These results therefore support a psychostimulant activity of modafinil in man.

scholarly journals Age-Related Cognitive Impairment: Role of Reduced Synaptobrevin-2 Levels in Deficits of Memory and Synaptic Plasticity

2019 ◽  
Vol 75 (9) ◽  
pp. 1624-1632 ◽  
Author(s):  
Albert Orock ◽  
Sreemathi Logan ◽  
Ferenc Deak
Keyword(s):  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Receptor Protein ◽  
Protein Levels ◽  
Ca1 Region ◽  
Age Related ◽  
Term Potentiation

AbstractCognitive impairment in the aging population is quickly becoming a health care priority, for which currently no disease-modifying treatment is available. Multiple domains of cognition decline with age even in the absence of neurodegenerative diseases. The cellular and molecular changes leading to cognitive decline with age remain elusive. Synaptobrevin-2 (Syb2), the major vesicular SNAP receptor protein, highly expressed in the cerebral cortex and hippocampus, is essential for synaptic transmission. We have analyzed Syb2 protein levels in mice and found a decrease with age. To investigate the functional consequences of lower Syb2 expression, we have used adult Syb2 heterozygous mice (Syb2+/−) with reduced Syb2 levels. This allowed us to mimic the age-related decrease of Syb2 in the brain in order to selectively test its effects on learning and memory. Our results show that Syb2+/− animals have impaired learning and memory skills and they perform worse with age in the radial arm water maze assay. Syb2+/− hippocampal neurons have reduced synaptic plasticity with reduced release probability and impaired long-term potentiation in the CA1 region. Syb2+/− neurons also have lower vesicular release rates when compared to WT controls. These results indicate that reduced Syb2 expression with age is sufficient to cause cognitive impairment.

scholarly journals Sleep Deprivation Causes Behavioral, Synaptic, and Membrane Excitability Alterations in Hippocampal Neurons

2003 ◽  
Vol 23 (29) ◽  
pp. 9687-9695 ◽  
Author(s):  
Carmel M. McDermott ◽  
Gerald J. LaHoste ◽  
Chu Chen ◽  
Alberto Musto ◽  
Nicolas G. Bazan ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Hippocampal Neurons ◽  
Membrane Excitability

scholarly journals 0429 Chronic Sleep Disturbance Causes Cognitive Impairment and Alzheimer’S Disease-Like Neuropathology

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A164-A164
Author(s):  
W Le
Keyword(s):  
Cognitive Impairment ◽  
Sleep Deprivation ◽  
Sleep Disturbance ◽  
Neuronal Apoptosis ◽  
Senile Plaques ◽  
Clinical Problem ◽  
Geriatric Population ◽  
Dementia Risk ◽  
Neuropsychological Functions ◽  
Chronic Sleep

Abstract Introduction Sleep disturbance is among the most common clinical problem and possesses a significant concern for the geriatric population. Recently, increasing evidence has indicated that disturbed sleep may not only affect neuropsychological functions, but also contribute to the cognitive impairment and, therefore, significantly increase dementia risk. Methods In the present study, we examined the potential impacts of chronic sleep deprivation (SD) on learning-memory and AD-related pathologies in AβPPswe/PS1ΔE9 transgenic (TG) mice and their wild-type (WT) littermates. Results Our results indicated that mice (both TG and WT) exposed to 2-month SD showed an altered amyloid-βprotein precursor processing, elevated level of phosphorylated tau protein, and impaired cognitive performance as compared to non-sleep deprivation (NSD) controls. Moreover, the SD-treated TG mice exhibited more amyloid-β1-42 production and developed more senile plaques in the cortex and hippocampus than NSD-treated TG mice. In addition, SD caused a striking neuronal mitochondrial damage, caspase cascade activation, and neuronal apoptosis in the hippocampus of both TG and WT mice. More importantly, all these behavioral, neuropathological, and biochemical changes induced by chronic SD were long lasting and were irreversible during a 3-month normal housing condition. Conclusion Collectively, these results indicate that chronic SD impairs learning and memory, exacerbates AD pathologies, and aggravates the mitochondria-mediated neuronal apoptosis in a long-lasting manner. Support Our findings provide important experimental evidence to prove that chronic sleep disturbance is a risk factor for AD.

scholarly journals Sleep Deprivation Induces Cognitive Impairment by Increasing Blood-Brain Barrier Permeability via CD44

2020 ◽  
Vol 11 ◽  
Author(s):  
Jing Sun ◽  
Jusheng Wu ◽  
Fuzhou Hua ◽  
Yong Chen ◽  
Fenfang Zhan ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Sleep Deprivation ◽  
Rna Sequencing ◽  
Blood Brain Barrier ◽  
Nervous System Development ◽  
Brain Barrier ◽  
Receptor Interaction ◽  
Blood Brain ◽  
Bbb Permeability

Sleep deprivation occurs frequently in older adults, which can result in delirium and cognitive impairment. CD44 is a key molecular in blood-brain barrier (BBB) regulation. However, whether CD44 participates in the role of sleep deprivation in cognitive impairment remains unclear. In this study, the effect of sleep deprivation on cognitive ability, tissue inflammation, BBB permeability, and astrocyte activity were evaluated in vivo. The differentially expressed genes (DEGs) were identified by RNA sequencing. A CD44 overexpression in the BBB model was performed in vitro to assess the effect and mechanisms of CD44. Sleep deprivation impaired the learning and memory ability and increased the levels of inflammatory cytokines, along with increased BBB permeability and activated astrocytes in hippocampus tissue. RNA sequencing of the hippocampus tissue revealed that 329 genes were upregulated in sleep deprivation-induced mice compared to control mice, and 147 genes were downregulated. GO and pathways showed that DEGs were mainly involved in BBB permeability and astrocyte activation, including nervous system development, neuron development, and brain development, and neuroactive ligand-receptor interaction. Moreover, the PCR analysis revealed that CD44 was dramatically increased in mice with sleep deprivation induction. The overexpression of CD44 in astrocytes promoted BBB permeability in vitro and induced the expression of the downstream gene NANOG. Our results indicate that sleep deprivation upregulated CD44 expression in hippocampus tissue, and increased BBB permeability, resulting in cognitive impairment.

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