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

IF 1.9 4区医学 Q3 PHYSIOLOGY

Respiratory Physiology & Neurobiology 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

Respiratory Physiology & Neurobiology 医学-呼吸系统

CiteScore

4.80

自引率

8.70%

发文量

104

审稿时长

54 days

期刊介绍： Respiratory Physiology & Neurobiology (RESPNB) publishes original articles and invited reviews concerning physiology and pathophysiology of respiration in its broadest sense. Although a special focus is on topics in neurobiology, high quality papers in respiratory molecular and cellular biology are also welcome, as are high-quality papers in traditional areas, such as: -Mechanics of breathing- Gas exchange and acid-base balance- Respiration at rest and exercise- Respiration in unusual conditions, like high or low pressure or changes of temperature, low ambient oxygen- Embryonic and adult respiration- Comparative respiratory physiology. Papers on clinical aspects, original methods, as well as theoretical papers are also considered as long as they foster the understanding of respiratory physiology and pathophysiology.