Contribution of orexin in hypercapnic chemoreflex: evidence from genetic and pharmacological disruption and supplementation studies in mice.

Contribution of orexin in hypercapnic chemoreflex: evidence from genetic and pharmacological disruption and supplementation studies in mice. Research Abstract Details 

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Contribution of orexin in hypercapnic chemoreflex: evidence from genetic and pharmacological disruption and supplementation studies in mice. Abstract Text:

Ben-Shiang Deng,Akira Nakamura,Wei Zhang,Masashi Yanagisawa,Yasuichiro Fukuda,Tomoyuki Kuwaki,Ben-Shiang Deng,Akira Nakamura,Wei Zhang,Masashi Yanagisawa,Yasuichiro Fukuda,Tomoyuki Kuwaki,Ben-Shiang Deng,Akira Nakamura,Wei Zhang,Masashi Yanagisawa,Yasuichiro Fukuda,Tomoyuki Kuwaki,

We have previously shown that hypercapnic chemoreflex in prepro-orexin knockout mice (ORX-KO) is attenuated during wake but not sleep periods. In that study, however, hypercapnic stimulation had been chronically applied for 6 h because of technical difficulty in changing the composition of the inspired gas mixture without distorting the animal's vigilance states. In the present study we examined possible involvement of orexin in acute respiratory chemoreflex during wake periods. Ventilation was recorded together with electroencephalography and electromyography before and after intracerebroventricular administration of orexin or an orexin receptor antagonist, SB-334867. A hypercapnic (5 or 10% CO(2)) or hypoxic (15 or 10% O(2)) gas mixture was introduced into the recording chamber for 5 min. Respiratory parameters were analyzed only for quiet wakefulness. When mice breathed normal room air, orexin-A and orexin-B but not vehicle or SB-334867 increased minute ventilation in both ORX-KO and wild-type (WT) mice. As expected, hypercapnic chemoreflex in vehicle-treated ORX- KO mice (0.22 +/- 0.03 ml.min(-1).g(-1).% CO(2)(-1)) was significantly blunted compared with that in WT mice (0.51 +/- 0.05 ml.min(-1).g(-1).% CO(2)(-1)). Supplementation of orexin-A or -B (3 nmol) partially restored the hypercapnic chemoreflex in ORX-KO mice (0.28 +/- 0.03 ml.min(-1).g(-1).% CO(2)(-1) for orexin-A and 0.32 +/- 0.04 ml.min(-1).g(-1).% CO(2)(-1) for orexin-B). In addition, injection of SB-334867 (30 nmol) in WT mice decreased the hypercapnic chemoreflex (0.39 +/- 0.04 ml.min(-1).g(-1).% CO(2)(-1)). On the other hand, hypoxic chemoreflex in vehicle-treated ORX-KO and SB-334867-treated WT mice was not different from that in corresponding controls. Our findings suggest that orexin plays a crucial role in CO(2) sensitivity at least during wake periods in mice.

Contribution of orexin in hypercapnic chemoreflex: evidence from genetic and pharmacological disruption and supplementation studies in mice. Publishing Authors By Initials

BS Deng,A Nakamura,W Zhang,M Yanagisawa,Y Fukuda,T Kuwaki,BS Deng,A Nakamura,W Zhang,M Yanagisawa,Y Fukuda,T Kuwaki,BS Deng,A Nakamura,W Zhang,M Yanagisawa,Y Fukuda,T Kuwaki,

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Contribution of orexin in hypercapnic chemoreflex: evidence from genetic and pharmacological disruption and supplementation studies in mice. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of applied physiology (Bethesda, Md. : 198

VOLUME: 103

Page Numbers: 1772-9

Journal Abbreviation: J. Appl. Physiol.

ISSN: 8750-7587

DAY: 23

MONTH: 08

YEAR: 2007

Contribution of orexin in hypercapnic chemoreflex: evidence from genetic and pharmacological disruption and supplementation studies in mice. Information

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LANGUAGE: eng

NlmUniqueID: 8502536

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AFFILIATION: Dept. of Molecular & Integrative Physiology, Chiba Univ. Graduate School of Medicine, 1-8-1 Chuo-ku, Chiba 260-8670, Japan. kuwaki@faculty.chiba-u.jp).

Country: United States

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MEDLINETA: J Appl Physiol

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