Changes in the composition of brain interstitial ions control the sleep-wake cycle

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Changes in the composition of brain interstitial ions control the sleep-wake cycle. / Ding, Fengfei; O'Donnell, John; Xu, Qiwu; Kang, Ning; Goldman, Nanna; Nedergaard, Maiken.

In: Science, Vol. 352, No. 6285, 29.04.2016, p. 550-555.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Ding, F, O'Donnell, J, Xu, Q, Kang, N, Goldman, N & Nedergaard, M 2016, 'Changes in the composition of brain interstitial ions control the sleep-wake cycle', Science, vol. 352, no. 6285, pp. 550-555. https://doi.org/10.1126/science.aad4821

APA

Ding, F., O'Donnell, J., Xu, Q., Kang, N., Goldman, N., & Nedergaard, M. (2016). Changes in the composition of brain interstitial ions control the sleep-wake cycle. Science, 352(6285), 550-555. https://doi.org/10.1126/science.aad4821

Vancouver

Ding F, O'Donnell J, Xu Q, Kang N, Goldman N, Nedergaard M. Changes in the composition of brain interstitial ions control the sleep-wake cycle. Science. 2016 Apr 29;352(6285):550-555. https://doi.org/10.1126/science.aad4821

Author

Ding, Fengfei ; O'Donnell, John ; Xu, Qiwu ; Kang, Ning ; Goldman, Nanna ; Nedergaard, Maiken. / Changes in the composition of brain interstitial ions control the sleep-wake cycle. In: Science. 2016 ; Vol. 352, No. 6285. pp. 550-555.

Bibtex

@article{3f425b62ade1427db3fad525d3686a8d,

title = "Changes in the composition of brain interstitial ions control the sleep-wake cycle",

abstract = "Wakefulness is driven by the widespread release of neuromodulators by the ascending arousal system. Yet, it is unclear how these substances orchestrate state-dependent, global changes in neuronal activity. Here, we show that neuromodulators induce increases in the extracellular K+ concentration ([K+]e) in cortical slices electrically silenced by tetrodotoxin. In vivo, arousal was linked to AMPA receptor-independent elevations of [K+]e concomitant with decreases in [Ca2+]e, [Mg2+]e, [H+]e, and the extracellular volume. Opposite, natural sleep and anesthesia reduced [K+]e while increasing [Ca2+]e, [Mg2+]e, and [H+]e as well as the extracellular volume. Local cortical activity of sleeping mice could be readily converted to the stereotypical electroencephalography pattern of wakefulness by simply imposing a change in the extracellular ion composition. Thus, extracellular ions control the state-dependent patterns of neural activity.",

keywords = "Animals, Calcium, Cations, Cerebral Cortex, Electroencephalography, Magnesium, Male, Mice, Mice, Inbred C57BL, Neurons, Neurotransmitter Agents, Potassium, Receptors, AMPA, Sleep, Sodium Channel Blockers, Tetrodotoxin, Wakefulness, Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, Non-P.H.S.",

author = "Fengfei Ding and John O'Donnell and Qiwu Xu and Ning Kang and Nanna Goldman and Maiken Nedergaard",

note = "Copyright {\textcopyright} 2016, American Association for the Advancement of Science.",

year = "2016",

month = apr,

day = "29",

doi = "10.1126/science.aad4821",

language = "English",

volume = "352",

pages = "550--555",

journal = "Science",

issn = "0036-8075",

publisher = "American Association for the Advancement of Science",

number = "6285",

}

RIS

TY - JOUR

T1 - Changes in the composition of brain interstitial ions control the sleep-wake cycle

AU - Ding, Fengfei

AU - O'Donnell, John

AU - Xu, Qiwu

AU - Kang, Ning

AU - Goldman, Nanna

AU - Nedergaard, Maiken

PY - 2016/4/29

Y1 - 2016/4/29

N2 - Wakefulness is driven by the widespread release of neuromodulators by the ascending arousal system. Yet, it is unclear how these substances orchestrate state-dependent, global changes in neuronal activity. Here, we show that neuromodulators induce increases in the extracellular K+ concentration ([K+]e) in cortical slices electrically silenced by tetrodotoxin. In vivo, arousal was linked to AMPA receptor-independent elevations of [K+]e concomitant with decreases in [Ca2+]e, [Mg2+]e, [H+]e, and the extracellular volume. Opposite, natural sleep and anesthesia reduced [K+]e while increasing [Ca2+]e, [Mg2+]e, and [H+]e as well as the extracellular volume. Local cortical activity of sleeping mice could be readily converted to the stereotypical electroencephalography pattern of wakefulness by simply imposing a change in the extracellular ion composition. Thus, extracellular ions control the state-dependent patterns of neural activity.

AB - Wakefulness is driven by the widespread release of neuromodulators by the ascending arousal system. Yet, it is unclear how these substances orchestrate state-dependent, global changes in neuronal activity. Here, we show that neuromodulators induce increases in the extracellular K+ concentration ([K+]e) in cortical slices electrically silenced by tetrodotoxin. In vivo, arousal was linked to AMPA receptor-independent elevations of [K+]e concomitant with decreases in [Ca2+]e, [Mg2+]e, [H+]e, and the extracellular volume. Opposite, natural sleep and anesthesia reduced [K+]e while increasing [Ca2+]e, [Mg2+]e, and [H+]e as well as the extracellular volume. Local cortical activity of sleeping mice could be readily converted to the stereotypical electroencephalography pattern of wakefulness by simply imposing a change in the extracellular ion composition. Thus, extracellular ions control the state-dependent patterns of neural activity.

KW - Animals

KW - Calcium

KW - Cations

KW - Cerebral Cortex

KW - Electroencephalography

KW - Magnesium

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Neurons

KW - Neurotransmitter Agents

KW - Potassium

KW - Receptors, AMPA

KW - Sleep

KW - Sodium Channel Blockers

KW - Tetrodotoxin

KW - Wakefulness

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, U.S. Gov't, Non-P.H.S.

U2 - 10.1126/science.aad4821

DO - 10.1126/science.aad4821

M3 - Journal article

C2 - 27126038

VL - 352

SP - 550

EP - 555

JO - Science

JF - Science

SN - 0036-8075

IS - 6285

ER -

ID: 164971851

Center for Translational Neuromedicine