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Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity.

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Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity. / SheikhBahaei, Shahriar; Turovsky, EA; Hosford, Patrick et al.
In: Nature Communications, Vol. 9, 370, 25.01.2018.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

SheikhBahaei, S, Turovsky, EA, Hosford, P, Hadjihambi, A, Theparambil, SM, Liu, B, Marina, N, Teschemacher, AG, Kasparov, S, Smith, JC & Gourine, A 2018, 'Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity.', Nature Communications, vol. 9, 370. https://doi.org/10.1038/s41467-017-02723-6

APA

SheikhBahaei, S., Turovsky, EA., Hosford, P., Hadjihambi, A., Theparambil, SM., Liu, B., Marina, N., Teschemacher, AG., Kasparov, S., Smith, JC., & Gourine, A. (2018). Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity. Nature Communications, 9, Article 370. https://doi.org/10.1038/s41467-017-02723-6

Vancouver

SheikhBahaei S, Turovsky EA, Hosford P, Hadjihambi A, Theparambil SM, Liu B et al. Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity. Nature Communications. 2018 Jan 25;9:370. doi: 10.1038/s41467-017-02723-6

Author

SheikhBahaei, Shahriar ; Turovsky, EA ; Hosford, Patrick et al. / Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity. In: Nature Communications. 2018 ; Vol. 9.

Bibtex

@article{7472659e9fe5405481b20da52d9f8fa9,
title = "Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity.",
abstract = "Astrocytes are implicated in modulation of neuronal excitability and synaptic function, but it remains unknown if these glial cells can directly control activities of motor circuits to influence complex behaviors in vivo. This study focused on the vital respiratory rhythm-generating circuits of the preB{\"o}tzinger complex (preB{\"o}tC) and determined how compromised function of local astrocytes affects breathing in conscious experimental animals (rats). Vesicular release mechanisms in astrocytes were disrupted by virally driven expression of either the dominant-negative SNARE protein or light chain of tetanus toxin. We show that blockade of vesicular release in preB{\"o}tC astrocytes reduces the resting breathing rate and frequency of periodic sighs, decreases rhythm variability, impairs respiratory responses to hypoxia and hypercapnia, and dramatically reduces the exercise capacity. These findings indicate that astrocytes modulate the activity of CNS circuits generating the respiratory rhythm, critically contribute to adaptive respiratory responses in conditions of increased metabolic demand and determine the exercise capacity.",
author = "Shahriar SheikhBahaei and EA Turovsky and Patrick Hosford and Anna Hadjihambi and SM Theparambil and B Liu and N Marina and AG Teschemacher and S Kasparov and JC Smith and Alexander Gourine",
year = "2018",
month = jan,
day = "25",
doi = "10.1038/s41467-017-02723-6",
language = "English",
volume = "9",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity.

AU - SheikhBahaei, Shahriar

AU - Turovsky, EA

AU - Hosford, Patrick

AU - Hadjihambi, Anna

AU - Theparambil, SM

AU - Liu, B

AU - Marina, N

AU - Teschemacher, AG

AU - Kasparov, S

AU - Smith, JC

AU - Gourine, Alexander

PY - 2018/1/25

Y1 - 2018/1/25

N2 - Astrocytes are implicated in modulation of neuronal excitability and synaptic function, but it remains unknown if these glial cells can directly control activities of motor circuits to influence complex behaviors in vivo. This study focused on the vital respiratory rhythm-generating circuits of the preBötzinger complex (preBötC) and determined how compromised function of local astrocytes affects breathing in conscious experimental animals (rats). Vesicular release mechanisms in astrocytes were disrupted by virally driven expression of either the dominant-negative SNARE protein or light chain of tetanus toxin. We show that blockade of vesicular release in preBötC astrocytes reduces the resting breathing rate and frequency of periodic sighs, decreases rhythm variability, impairs respiratory responses to hypoxia and hypercapnia, and dramatically reduces the exercise capacity. These findings indicate that astrocytes modulate the activity of CNS circuits generating the respiratory rhythm, critically contribute to adaptive respiratory responses in conditions of increased metabolic demand and determine the exercise capacity.

AB - Astrocytes are implicated in modulation of neuronal excitability and synaptic function, but it remains unknown if these glial cells can directly control activities of motor circuits to influence complex behaviors in vivo. This study focused on the vital respiratory rhythm-generating circuits of the preBötzinger complex (preBötC) and determined how compromised function of local astrocytes affects breathing in conscious experimental animals (rats). Vesicular release mechanisms in astrocytes were disrupted by virally driven expression of either the dominant-negative SNARE protein or light chain of tetanus toxin. We show that blockade of vesicular release in preBötC astrocytes reduces the resting breathing rate and frequency of periodic sighs, decreases rhythm variability, impairs respiratory responses to hypoxia and hypercapnia, and dramatically reduces the exercise capacity. These findings indicate that astrocytes modulate the activity of CNS circuits generating the respiratory rhythm, critically contribute to adaptive respiratory responses in conditions of increased metabolic demand and determine the exercise capacity.

U2 - 10.1038/s41467-017-02723-6

DO - 10.1038/s41467-017-02723-6

M3 - Journal article

C2 - 29371650

VL - 9

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 370

ER -