Replies to Commentaries on ATP Changes During Sleep

Dworak, Markus; McCarley, Robert W.; Kim, Tae; Kalinchuk, Anna V.; Basheer, Radhika

doi:10.5665/sleep.1110

Cited by 7 publications

(6 citation statements)

References 35 publications

(38 reference statements)

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“…Our data are in agreement with previous observations showing that neuronal signaling is metabolically expensive (Attwell and Laughlin, 2001, Attwell and Gibb, 2005) and that periods of neuronal slowdown increase the availability of high energy molecules such as ATP (Dworak et al, 2007, 2010, 2011a,b). …”

Section: Discussionsupporting

confidence: 93%

“…This increase in brain energy consumption with PSPs is a function of the increased activity of the sodium-potassium pump (Na + -K + -ATPase) which is activated by the influx of sodium ions and efflux of potassium ions accompanying PSP or action potential depolarizations. In contrast, periods of decreased neuronal activity, as observed during spontaneous sleep or some forms of anesthesia might reduce brain energy demand and conserve brain energy (Dworak et al, 2007, 2010, 2011a,b). These periods of reduced neuronal activity are characterized by delta oscillations (0.5–4.5 Hz), with each delta wave comprised of a prolonged (0.2-0.8s) hyperpolarization followed by a brief burst of action potentials (Steriade et al, 1993a, Steriade et al, 1993b, Steriade and McCarley, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Delta oscillations induced by ketamine increase energy levels in sleep-wake related brain regions

et al. 2011

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Neuronal signaling consumes much of the brain energy, mainly through the restoration of the membrane potential (MP) by ATP-consuming ionic pumps. We have reported that, compared with waking, ATP levels increase during the initial hours of natural slow-wave sleep, a time with prominent EEG delta oscillations (0.5-4.5Hz). We have hypothesized that there is a delta oscillation-ATP increase coupling, since, during delta waves, neurons exhibit a prolonged hyperpolarizing phase followed by a very brief phase of action potentials. However, direct proof of this hypothesis is lacking, and rapid changes in EEG/ neuronal activity preclude measurement in the naturally sleeping brain. Thus, to induce a uniform state with pure delta oscillations and one previously shown to be accompanied by a similar pattern of neuronal activity during delta waves as natural sleep, we used ketamine-xylazine treatment in rats. We here report that, with this treatment, the high energy molecules ATP and ADP increased in frontal and cingulate cortices, basal forebrain, and hippocampus compared with spontaneous waking. Moreover, the degree of ATP increase positively and significantly correlated with the degree of EEG delta-activity. Supporting the hypothesis of decreased ATP consumption during delta activity, the ATP-consuming Na+-K+-ATPase mRNA levels were significantly decreased whereas the mRNAs for the ATP-producing cytochrome c oxidase (COX) subunits COX III and COX IVa were unchanged. Taken together, these data support the hypothesis of a cortical delta oscillation-dependent reduction in ATP consumption, thus providing the brain with increased ATP availability, and likely occurring because of reduced Na+-K+-ATPase related energy consumption.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Delta oscillations induced by ketamine increase energy levels in sleep-wake related brain regions

et al. 2011

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“…P2X7R is an ATP-gated ionotropic channel implicated in sleep regulation and as well as the regulation of various neuronal functions, such as neurotransmitter release and synaptic transmission, and contributing to the formation of network oscillations (Jimenez-Mateos et al, 2019;Ribeiro et al, 2019). ATP is released with neuro-and glio-transmission, and neuronal activity is greater during wakefulness (Dworak et al, 2010). Thus, inhibiting P2X7R leads to decreased wakefulness, consistent with our research.…”

Section: Discussionsupporting

confidence: 88%

P2X7 receptor-activated microglia in cortex is critical for sleep disorder under neuropathic pain

Gao²,

He³

et al. 2023

Front. Neurosci.

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Neuropathic pain (NP) is associated with sleep disturbances, which may substantially influence the quality of life. Clinical and animal studies demonstrated that neurotransmitter is one of the main contributors to cause sleep disturbances induced by NP. Recently, it was reported that P2X7 receptors (P2X7R) are widely expressed in microglia, which serves crucial role in neuronal activity in the pain and sleep-awake cycle. In this study, we adopted the chronic constriction injury (CCI) model to establish the progress of chronic pain and investigated whether P2X7R of microglia in cortex played a critical role in sleep disturbance induced by NP. At electroencephalogram (EEG) level, sleep disturbance was observed in mice treated with CCI as they exhibited mechanical and thermal hypersensitivity, and inhibition of P2X7R ameliorated these changes. We showed a dramatic high level of P2X7R and Iba-1 co-expression in the cortical region, and the inhibition of P2X7R also adversely affected it. Furthermore, the power of LFPs in ventral posterior nucleus (VP) and primary somatosensory cortex (S1) which changed in the CCI group was adverse after the inhibition of P2X7R. Furthermore, inhibition of P2X7R also decreased the VP-S1 coherence which increased in CCI group. Nuclear magnetic resonance demonstrated inhibition of P2X7R decreased glutamate (Glu) levels in thalamic and cortical regions which were significantly increased in the CCI mice. Our findings provide evidence that NP has a critical effect on neuronal activity linked to sleep and may built up a new target for the development of sleep disturbances under chronic pain conditions.

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“…Furthermore, intracellular ATP concentrations are~10,000 times higher than adenosine concentrations; thus substantial changes in ATP-derived adenosine can occur without greatly affecting intracellular ATP levels (39). Accurate measurements of nucleotides, nucleosides, and their metabolites are technically challenging and controversial (8,17,22,25,27,40,67,69). Regardless, extracellular ATP in the brain extracellular fluid is derived from the release of ATP from neurons and glia as a consequence of cellular activity.…”

mentioning

confidence: 99%

P2X7 receptors in body temperature, locomotor activity, and brain mRNA and lncRNA responses to sleep deprivation

Davis

Taishi

Honn

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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The ionotropic purine type 2X7 receptor (P2X7R) is a nonspecific cation channel implicated in sleep regulation and brain cytokine release. Many endogenous rhythms covary with sleep, including locomotor activity and core body temperature. Furthermore, brain-hypothalamic cytokines and purines play a role in the regulation of these physiological parameters as well as sleep. We hypothesized that these parameters are also affected by the absence of the P2X7 receptor. Herein, we determine spontaneous expression of body temperature and locomotor activity in wild-type (WT) and P2X7R knockout (KO) mice and how they are affected by sleep deprivation (SD). We also compare hypothalamic, hippocampal, and cortical cytokine- and purine-related receptor and enzyme mRNA expressions before and after SD in WT and P2X7RKO mice. Next, in a hypothesis-generating survey of hypothalamic long noncoding (lnc) RNAs, we compare lncRNA expression levels between strains and after SD. During baseline conditions, P2X7RKO mice had attenuated temperature rhythms compared with WT mice, although locomotor activity patterns were similar in both strains. After 6 h of SD, body temperature and locomotion were enhanced to a greater extent in P2X7RKO mice than in WT mice during the initial 2-3 h after SD. Baseline mRNA levels of cortical TNF-α and P2X4R were higher in the KO mice than WT mice. In response to SD, the KO mice failed to increase hypothalamic adenosine deaminase and P2X4R mRNAs. Further, hypothalamic lncRNA expressions varied by strain, and with SD. Current data are consistent with a role for the P2X7R in thermoregulation and lncRNA involvement in purinergic signaling.

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Replies to Commentaries on ATP Changes During Sleep

Cited by 7 publications

References 35 publications

Delta oscillations induced by ketamine increase energy levels in sleep-wake related brain regions

Delta oscillations induced by ketamine increase energy levels in sleep-wake related brain regions

P2X7 receptor-activated microglia in cortex is critical for sleep disorder under neuropathic pain

P2X7 receptors in body temperature, locomotor activity, and brain mRNA and lncRNA responses to sleep deprivation

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