Extracellular adenosine and slow-wave sleep are increased after ablation of nucleus accumbens core astrocytes and neurons in mice

Zhou, Xiao-cong; Oishi, Yo; Chérasse, Yoan; Korkutata, Mustafa; Fujii, Shinya; Lee, Chia‐Ying; Lazarus, Michael

doi:10.1016/j.neuint.2019.01.020

Cited by 17 publications

(17 citation statements)

References 105 publications

(129 reference statements)

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“…The same genetic manipulation suppressed the LPS-induced increase in slow-wave power during NREM sleep, proving the astroglial contribution to inflammatory-derived increased sleep pressure ( 365 ). Although the role of A2 receptor (A2R) activation by astroglial adenosine is still controversial, A2Rs may play a role in sleep homeostasis through activation of A2AR-expressing neurons in the nucleus accumbens core involved in the induction of slow-wave sleep ( 366 ). In the cortex, altered gliotransmission resulted in reduced neuronal NMDA receptor activity and reduced slow oscillations ( 367 ), whereas astroglial specific activation induced neuronal transition to slow oscillations ( 368 ).…”

Section: Absence Seizures and Nrem Sleep: Two Sides Of The Same Coin?mentioning

confidence: 99%

From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research

2021

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The electrographic hallmark of childhood absence epilepsy (CAE) and other idiopathic forms of epilepsy are 2.5–4 Hz spike and wave discharges (SWDs) originating from abnormal electrical oscillations of the cortico-thalamo-cortical network. SWDs are generally associated with sudden and brief non-convulsive epileptic events mostly generating impairment of consciousness and correlating with attention and learning as well as cognitive deficits. To date, SWDs are known to arise from locally restricted imbalances of excitation and inhibition in the deep layers of the primary somatosensory cortex. SWDs propagate to the mostly GABAergic nucleus reticularis thalami (NRT) and the somatosensory thalamic nuclei that project back to the cortex, leading to the typical generalized spike and wave oscillations. Given their shared anatomical basis, SWDs have been originally considered the pathological transition of 11–16 Hz bursts of neural oscillatory activity (the so-called sleep spindles) occurring during Non-Rapid Eye Movement (NREM) sleep, but more recent research revealed fundamental functional differences between sleep spindles and SWDs, suggesting the latter could be more closely related to the slow (<1 Hz) oscillations alternating active (Up) and silent (Down) cortical activity and concomitantly occurring during NREM. Indeed, several lines of evidence support the fact that SWDs impair sleep architecture as well as sleep/wake cycles and sleep pressure, which, in turn, affect seizure circadian frequency and distribution. Given the accumulating evidence on the role of astroglia in the field of epilepsy in the modulation of excitation and inhibition in the brain as well as on the development of aberrant synchronous network activity, we aim at pointing at putative contributions of astrocytes to the physiology of slow-wave sleep and to the pathology of SWDs. Particularly, we will address the astroglial functions known to be involved in the control of network excitability and synchronicity and so far mainly addressed in the context of convulsive seizures, namely (i) interstitial fluid homeostasis, (ii) K+ clearance and neurotransmitter uptake from the extracellular space and the synaptic cleft, (iii) gap junction mechanical and functional coupling as well as hemichannel function, (iv) gliotransmission, (v) astroglial Ca2+ signaling and downstream effectors, (vi) reactive astrogliosis and cytokine release.

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Section: Absence Seizures and Nrem Sleep: Two Sides Of The Same Coin?mentioning

confidence: 99%

From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research

2021

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“…Cholinergic neurons in the basal forebrain, histaminergic neurons, and hypocretin in the hypothalamus, monoaminergic neuron (dopamine, 5‐hydroxytryptamine, norepinephrine) in the brainstem send out fibers that constitute the ascending reticular activation system (ARAS), which plays a role in cortical arousal . In addition, adenosine can also activate GABA neurons by reducing GABA inputs in the ventrolateral preoptic nucleus (VLPO) for sleep induction, and inhibit glutamate neurons in cerebral cortex, striatum, hippocampus, and other brain regions to achieve the coordination between different sleep behaviors …”

Section: The Role Of Adenosine and Its Receptors In Central Nervous Smentioning

confidence: 99%

Research progress on adenosine in central nervous system diseases

et al. 2019

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As an endogenous neuroprotectant agent, adenosine is extensively distributed and is particularly abundant in the central nervous system (CNS). Under physiological conditions, the concentration of adenosine is low intra‐ and extracellularly, but increases significantly in response to stress. The majority of adenosine functions are receptor‐mediated, and primarily include the A1, A2A, A2B, and A3 receptors (A1R, A2AR, A2BR, and A3R). Adenosine is currently widely used in the treatment of diseases of the CNS and the cardiovascular systems, and the mechanisms are related to the disease types, disease locations, and the adenosine receptors distribution in the CNS. For example, the main infarction sites of cerebral ischemia are cortex and striatum, which have high levels of A1 and A2A receptors. Cerebral ischemia is manifested with A1R decrease and A2AR increase, as well as reduction in the A1R‐mediated inhibitory processes and enhancement of the A2AR‐mediated excitatory process. Adenosine receptor dysfunction is also involved in the pathology of Alzheimer's disease (AD), depression, and epilepsy. Thus, the adenosine receptor balance theory is important for brain disease treatment. The concentration of adenosine can be increased by endogenous or exogenous pathways due to its short half‐life and high inactivation properties. Therefore, we will discuss the function of adenosine and its receptors, adenosine formation, and metabolism, and its role for the treatment of CNS diseases (such as cerebral ischemia, AD, depression, Parkinson's disease, epilepsy, and sleep disorders). This article will provide a scientific basis for the development of novel adenosine derivatives through adenosine structure modification, which will lead to experimental applications.

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“…70 Moreover, experimental activation of astrocytes, and thus induction of calcium transients, results in slow oscillations which have been shown to be important in sleep and memory formation. [71][72][73] Therefore, it is plausible that astrocyte dysfunction observed in CID impairs astrocytes sleep-regulating capabilities. On the other hand, sleep has been proposed to be "the brain's housekeeper", serving to restore and repair the brain.…”

Section: Gfapmentioning

confidence: 99%

<p>Astroglial Mechanisms Underlying Chronic Insomnia Disorder: A Clinical Study</p>

Zhang¹,

Li²,

Zhang³

et al. 2020

NSS

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The objective of this study was to investigate whether the serum biomarkers S100 calcium binding protein B (S100B), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF), and glial cell line-derived neurotrophic factor (GDNF) change in patients with chronic insomnia disorder (CID), and if this is the case, whether the altered levels of these serum biomarkers are associated with poor sleep quality and cognitive decline in CID. Patients and Methods: Fifty-seven CID outpatients constituted the CID group; thirty healthy controls (HC) were also enrolled. Questionnaires, polysomnography, Chinese-Beijing Version of Montreal Cognitive Assessment (MoCA-C) and Nine Box Maze Test (NBMT) were used to assess their sleep and neuropsychological function. Serum S100B, GFAP, BDNF, and GDNF were evaluated using enzyme-linked immunosorbent assay. Results: The CID group had higher levels of S100B and GFAP and lower levels of BDNF and GDNF than the HC group. Spearman correlation analysis revealed that poor sleep quality, assessed by subjective and objective measures, was positively correlated with S100B level and negatively correlated with BDNF level. GFAP level correlated positively with poor subjective sleep quality. Moreover, S100B and GFAP levels correlated negatively with general cognitive function assessed using MoCA-C. GFAP level correlated positively with poor spatial working memory (SWM) in the NBMT; BDNF level was linked to poor SWM and object recognition memory (ORcM) in the NBMT. However, principal component analysis revealed that serum S100B level was positively linked to the errors in object working memories, BDNF and GDNF concentrations were negatively linked with errors in ORcM, and GFAP concentration was positively correlated with the errors in the SWM and spatial reference memories. Conclusion: Serum S100B, GFAP, BDNF, and GDNF levels were altered in patients with CID, indicating astrocyte damage, and were associated with insomnia severity or/and cognitive dysfunction.

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Extracellular adenosine and slow-wave sleep are increased after ablation of nucleus accumbens core astrocytes and neurons in mice

Cited by 17 publications

References 105 publications

From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research

From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research

Research progress on adenosine in central nervous system diseases

<p>Astroglial Mechanisms Underlying Chronic Insomnia Disorder: A Clinical Study</p>

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