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抑制机制通过限制旁呼气驱动来控制主动呼气。

Inhibitory mechanisms control active expiration by limiting parafacial expiratory drive.

机构信息

Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut.

出版信息

J Neurophysiol. 2021 Mar 1;125(3):858-861. doi: 10.1152/jn.00507.2020. Epub 2021 Jan 27.

Abstract

Activity of parafacial neurons that control active expiration is heavily dependent on tonic and CO/H-dependent excitatory and inhibitory inputs from yet poorly defined sources. Contrary to the idea that CO/H disinhibits parafacial expiratory neurons, the recent work of J. D. Silva et al. (Silva JD, Oliveira LM, Souza FC, Moreira TS, Takakura AC. 123: 1933-1943, 2020) suggests that GABAergic raphe neurons preferentially limit expiratory activity during high CO. Here, I discuss these findings and propose a model where GABAergic raphe neurons function as CO/H-dependent breaks on expiratory drive.

摘要

控制主动呼气的口旁核神经元的活动强烈依赖于尚未明确的来源的紧张性和 CO/H 依赖性兴奋性和抑制性输入。与 CO/H 去抑制口旁核呼气神经元的观点相反,最近 J.D. 席尔瓦等人的工作(Silva JD, Oliveira LM, Souza FC, Moreira TS, Takakura AC. 123: 1933-1943, 2020)表明, 5-羟色胺能中缝核神经元在高 CO 期间优先限制呼气活动。在这里,我讨论了这些发现,并提出了一个模型,其中 5-羟色胺能中缝核神经元作为 CO/H 依赖性呼气驱动的中断。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf89/7988754/191110c8d8f5/JN-00507-2020r01.jpg

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