Tonic inhibition of brown adipose tissue sympathetic nerve activity via muscarinic acetylcholine receptors in the rostral raphe pallidus.
Tonic inhibition of brown adipose tissue sympathetic nerve activity via muscarinic acetylcholine receptors in the rostral raphe pallidus.
复制标题
通过中缝苍白肌头端的毒蕈碱乙酰胆碱受体对棕色脂肪组织交感神经活动进行强直性抑制。
DOI：
10.1113/jp275299
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
Morrison,ShaunF
中科院分区：
文献类型：
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作者：
Conceição,EllenPaulaSantos;Madden,ChristopherJ;Morrison,ShaunF
毒蕈碱类胆碱能抑制吻侧raphe pallidus （rRPa）神经元的强直活性影响褐色脂肪组织（BAT）的产热，而不依赖于环境温度条件。对rRPa的强直活性胆碱能输入起源于下丘脑的尾侧。毒毒碱乙酰胆碱受体（mAChR）在rRPa中的激活有助于抑制由吻侧腹外侧髓质（RVLM）神经元激活引起的BAT交感神经活动（SNA）。RVLM不是向rRPa输入毒蕈碱胆碱能的唯一来源。rpa中GABA受体的激活不会介导BAT SNA的胆碱能抑制。摘要我们试图确定体温和能量消耗是否受到神经输入的胆碱能的影响，神经输入到吻侧raphe pallidus (rRPa)，交感前运动神经元控制棕色脂肪组织（BAT）的产热。在麻醉大鼠的rRPa中纳米注射毒毒碱型乙酰胆碱受体（mAChR）激动剂oxotremorine或胆碱酯酶抑制剂新斯的明（NEOS），可降低冷诱发的BAT交感神经活性（SNA，最低点：- 72和- 95%），BAT温度（Tbat, - 0.5和- 0.6°C）， CO2(Exp。CO2,−0.3和−0.5%)和心率（HR，−22和−41 bpm）。NEOS进入rRPa逆转了阻断rpa中GABA受体引起的BAT SNA的增加。在温暖大鼠的rRPa中纳米注射mAChR拮抗剂东莨菪碱（SCOP），使BAT SNA（峰值：+1087%）、tha（+1.8°C）、Exp. CO2（+0.7%）、核心温度（Tcore, +0.5°C）和HR （+54 bpm）升高。在低温暴露期间，在下丘脑尾侧脑横切之后，以及在rRPa中谷氨酸受体阻断期间，在rRPa中注射SCOP纳米注射产生了类似的BAT激活。我们得出结论，对rRPa的强直活性胆碱能输入通过激活局部mAChR抑制BAT SNA。mAChR在rRPa中介导的BAT SNA抑制并不依赖于rpa中GABA受体的激活。mAChR阻断rpa后，BAT SNA的增加不依赖于下丘脑神经元的活性或rpa中谷氨酸受体的激活。
Key pointsA tonically active, muscarinic cholinergic inhibition of rostral raphe pallidus (rRPa) neurons influences thermogenesis of brown adipose tissue (BAT) independent of ambient temperature conditions.The tonically active cholinergic input to rRPa originates caudal to the hypothalamus.Muscarinic acetylcholine receptor (mAChR) activation in rRPa contributes to the inhibition of BAT sympathetic nerve activity (SNA) evoked by activation of neurons in the rostral ventrolateral medulla (RVLM).The RVLM is not the sole source of the muscarinic cholinergic input to rRPa.Activation of GABA receptors in rRPa does not mediate the cholinergic inhibition of BAT SNA.AbstractWe sought to determine if body temperature and energy expenditure are influenced by a cholinergic input to neurons in the rostral raphe pallidus (rRPa), the site of sympathetic premotor neurons controlling thermogenesis of brown adipose tissue (BAT). Nanoinjections of the muscarinic acetylcholine receptor (mAChR) agonist, oxotremorine, or the cholinesterase inhibitor, neostigmine (NEOS), in the rRPa of anaesthetized rats decreased cold‐evoked BAT sympathetic nerve activity (SNA, nadirs: −72 and −95%), BAT temperature (Tbat, −0.5 and −0.6°C), expired CO2(Exp. CO2, −0.3 and −0.5%) and heart rate (HR, −22 and −41 bpm). NEOS into rRPa reversed the increase in BAT SNA evoked by blockade of GABA receptors in rRPa. Nanoinjections of the mAChR antagonist, scopolamine (SCOP), in the rRPa of warm rats increased BAT SNA (peak: +1087%), Tbat(+1.8°C), Exp. CO2(+0.7%), core temperature (Tcore, +0.5°C) and HR (+54 bpm). SCOP nanoinjections in rRPa produced similar activations of BAT during cold exposure, following a brain transection caudal to the hypothalamus, and during the blockade of glutamate receptors in rRPa. We conclude that a tonically active cholinergic input to the rRPa inhibits BAT SNA via activation of local mAChR. The inhibition of BAT SNA mediated by mAChR in rRPa does not depend on activation of GABA receptors in rRPa. The increase in BAT SNA following mAChR blockade in rRPa does not depend on the activity of neurons in the hypothalamus or on glutamate receptor activation in rRPa.