Disinhibition does not play a role in endomorphin-2-induced changes in inspiratory motoneuron output produced by in vitro neonatal rat preparations

IF 16.4 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY

Accounts of Chemical Research Pub Date : 2023-11-07 DOI:10.1016/j.resp.2023.104186

Stephen M. Johnson, Maia G. Gumnit, Sarah M. Johnson, Tracy L. Baker, Jyoti J. Watters

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引用次数: 0

Abstract

Low level activation of mu-opioid receptors (MORs) in neonatal rat brainstem-spinal cord preparations increases inspiratory burst amplitude recorded on cervical spinal roots. We tested whether: (1) MOR activation with an endogenous ligand, such as endomorphin-2, increases inspiratory burst amplitude, (2) disinhibition of GABAergic or glycinergic inhibitory synaptic transmission is involved, and (3) inflammation alters endomorphin-2 effects. Using neonatal rat (P0-P3) brainstem-spinal cord preparations, bath-applied endomorphin-2 (10–200 nM) increased inspiratory burst amplitude and decreased burst frequency. Blockade of GABAA receptors (picrotoxin), glycine receptors (strychnine), or both (picrotoxin and strychnine) did not abolish endomorphin-2-induced effects. In preparations isolated from neonatal rats injected 3 h previously with lipopolysaccharide (LPS, 0.1 mg/kg), endomorphin-2 continued to decrease burst frequency but abolished the burst amplitude increase. Collectively, these data indicate that disinhibition of inhibitory synaptic transmission is unlikely to play a role in endomorphin-2-induced changes in inspiratory motor output, and that different mechanisms underlie the endomorphin-2-induced increases in inspiratory burst amplitude and decreases in burst frequency.

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去抑制在体外新生大鼠制剂产生的内吗啡-2诱导的吸气运动神经元输出变化中不起作用。

新生大鼠脑干脊髓制剂中μ阿片受体（MORs）的低水平激活增加了颈脊髓根上记录的吸气爆发幅度。我们测试了：（1）用内源性配体（如内吗啡-2）激活MOR是否会增加吸气爆发幅度，（2）参与GABA能或甘氨酸能抑制性突触传递的去抑制，以及（3）炎症改变内吗啡-2的作用。使用新生大鼠（P0-P3）脑干脊髓制剂，浴中应用endomorpin-2（10-200nM）可增加吸气爆发幅度并降低爆发频率。阻断GABAA受体（苦rotoxin）、甘氨酸受体（士的宁）或两者（苦rotaxin和士的宁。在从预先注射脂多糖（LPS，0.1mg/kg）3h的新生大鼠分离的制剂中，内吗啡-2继续降低爆发频率，但消除了爆发幅度的增加。总之，这些数据表明，抑制性突触传递的去抑制不太可能在内源性吗啡-2诱导的吸气运动输出变化中发挥作用，并且不同的机制是内源性吗啡-2导致的吸气爆发幅度增加和爆发频率降低的基础。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.